RNA Sequencing Analysis of Monocytes Exposed to Airway Fluid from Children with Pediatric Acute Respiratory Distress Syndrome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1054078 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27254700_1.fastq.gz | Fastqsanger.gz | |||
| SRR27254700_2.fastq.gz | Fastqsanger.gz | |||
| SRR27254800_1.fastq.gz | Fastqsanger.gz | |||
| SRR27254800_2.fastq.gz | Fastqsanger.gz | |||
| SRR27254701_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 244 |
Similar Datasets
Project description:Importance: Monocytes are plastic cells that assume different polarization states that can either promote inflammation or tissue repair and inflammation resolution. Polarized monocytes are partially defined by their transcriptional profiles that are influenced by environmental stimuli. The airway monocyte response in pediatric acute respiratory distress syndrome (PARDS) is undefined. Objectives: To identify differentially expressed genes and networks using a novel transcriptomic reporter assay with donor monocytes exposed to the airway fluid of intubated children with and at-risk for PARDS. To determine differences in gene expression at two time points using the donor monocyte assay exposed to airway fluid from intubated children with PARDS obtained 48-96 hours following initial tracheal aspirate sampling. Design, Setting and Participants: In vitro pilot study carried out using airway fluid supernatant from 57 children: 44 children with PARDS and 13 children at-risk for PARDS. Main Outcomes and Measures: We performed bulk RNA sequencing using a transcriptomic reporter assay of monocytes exposed to airway fluid from intubated children to discover gene networks differentiating PARDS from at-risk for PARDS. We also report differences in gene expression in children with PARDS 48-96 hours following initial tracheal aspirate sampling. Results: We found that interleukin (IL)-10, -4, and -13, cytokine/chemokine signaling, and the senescence-associated secretory phenotype are upregulated in monocytes exposed to airway fluid from intubated children with PARDS compared to those at-risk for PARDS. Signaling by NOTCH, histone deacetylation/acetylation, DNA methylation, chromatin modifications (B-WICH complex), and RNA polymerase I transcription and its associated regulatory apparatus were upregulation in children with PARDS 48-96 hours following initial tracheal aspirate sampling. Conclusions and Relevance: We identified gene networks important to the PARDS airway immune response using bulk RNA sequencing from a monocyte reporter assay that exposed monocytes to airway fluid from intubated children with and at-risk for PARDS. Mechanistic investigations are needed to validate our findings.
2024-06-01 | GSE250448 | GEO
Project description:Intra-amniotic infection, the invasion of microbes into the amniotic cavity resulting in an inflammatory process, is a clinical condition that can lead to adverse pregnancy outcomes for the mother and fetus as well as severe long-term neonatal morbidities. Despite much research focused on the consequences of intra-amniotic infection, there is still little knowledge about the functional roles of innate immune cells that respond to invading microbes. In the current study, we performed RNA sequencing of sorted neutrophils and monocytes/macrophages from amniotic fluid from women with intra-amniotic infection to determine the transcriptomic differences between these innate immune cells. Further, we sought to identify specific transcriptomic pathways that were significantly altered by the maternal or fetal origin of amniotic fluid neutrophils and monocytes, the presence of a severe fetal inflammatory response, and pregnancy outcome (i.e. preterm or term delivery). We showed that significant transcriptomic differences exist between amniotic fluid neutrophils and monocytes/macrophages from women with intra-amniotic infection that are indicative of the distinct roles these cells play. We also found that amniotic fluid monocytes/macrophages of fetal origin display impaired ability to clear out microbes invading the amniotic cavity compared to those of maternal origin. Notably, we demonstrate that the transcriptomic changes in amniotic fluid monocytes/macrophages are heavily associated with the severity of the fetal inflammatory response, suggesting that the trafficking of fetal neutrophils throughout the umbilical cord is partially modulated by monocytes/macrophages in the amniotic cavity. Finally, we show that amniotic fluid neutrophils and monocytes/macrophages from preterm deliveries display enhanced transcriptomic activity compared to those from term deliveries, highlighting the protective role of these innate immune cells in this vulnerable period. Collectively, these findings demonstrate the underlying complexity of local innate immune responses in women with intra-amniotic infection, and provide new insights into the functions of amniotic fluid neutrophils and monocytes in the amniotic cavity.
2023-01-05 | GSE222204 | GEO
Project description:This project involves proteome characterization of healthy monocytes polarized (activated) with synovial fluid (SF) versus serum from patients with juvenile idiopathic arthritis (JIA). The objective is to investigate the influence of SF on monocytes at the proteome level, using serum polarized monocytes as a control. Monocytes were isolated from peripheral blood mononuclear cells of healthy donors following negative selection and were subsequently polarized overnight with 20% of a pool of either serum or SF. They were subsequently detached and used for proteome analysis.
2023-07-20 | PXD033983 | Pride
Project description:Pediatric acute respiratory distress syndrome (PARDS) is a heterogeneous illness affecting 6% of mechanically ventilated children and with an overall mortality of 17%. Studies in PARDS have mainly focused on plasma biomarkers which may not reflect airway biomarkers. We lack adequate understanding of the inflammatory mediators and underlying immune responses in the airways of PARDS patients. Our objective was to compare the levels of cytokines in the airway fluid of intubated children with severe versus nonsevere acute respiratory distress syndrome.DesignProspective observational cohort study.SettingSingle 36-bed quaternary care academic safety-net hospital PICU.PatientsChildren intubated for acute respiratory failure between January 2018 and November 2021 stratified by Pediatric Acute Lung Injury Consensus Conference-1 criteria for PARDS.InterventionsNone.Measurements and main resultsWe measured levels of 23 cytokines, chemokines, and protein biomarkers in the tracheal aspirate from 82 intubated children, between 14 days and 17 years old, at risk for or with PARDS. Levels of interleukin-4, -5, -7, -8, -12(p-70), -17a, -21, and fractalkine were higher in patients with severe versus nonsevere PARDS. There were no associations between airway and plasma cytokines.ConclusionsProinflammatory cytokines are elevated in the airway fluid from intubated children with severe PARDS and reflect diverse patterns of airway inflammation.
| S-EPMC9760621 | biostudies-literature
Project description:Rationale: Serial measurements of genome-wide transcriptional changes in alveolar macrophages (AM) and peripheral blood monocytes (PBM) from patients with acute respiratory distress (ARDS) could clarify the biologic programs activated in ARDS and the relationship of these changes to clinical outcomes. Objectives: To identify transcriptional programs activated in purified AM and PBM over the course of ARDS, and determine the relationship of these programs with patient outcomes. Methods: We performed transcriptional profiling of total RNA isolated from AMs and PBMs purified from bronchoalveolar lavage fluid (BALF) and peripheral blood respectively, collected from patients (n = 26) with ARDS previously enrolled in a phase-II clinical trial. Cells were obtained at baseline (day 0) after enrollment. Measurements and Main Results: Using an unbiased gene set enrichment analysis (GSEA), we found highly divergent patterns of gene expression in AMs and PBMs. Notably, immuno-inflammatory gene sets were enriched in AMs isolated on day 0 in those who survived and had more ventilator-free days (VFD); however, this association between inflammatory and immune gene sets and good outcomes was not seen in PBMs. Conclusion: Transcriptional responses during ARDS are remarkably different between AMs and PBMs. Rationale: Serial measurements of genome-wide transcriptional changes in alveolar macrophages (AM) and peripheral blood monocytes (PBM) from patients with acute respiratory distress (ARDS) could clarify the biologic programs activated in ARDS and the relationship of these changes to clinical outcomes. Objectives: To identify transcriptional programs activated in purified AM and PBM over the course of ARDS, and determine the relationship of these programs with patient outcomes. Methods: We performed transcriptional profiling of total RNA isolated from AMs and PBMs purified from bronchoalveolar lavage fluid and peripheral blood respectively, collected from patients (n = 26) with ARDS previously enrolled in a phase-II clinical trial. Cells were obtained at baseline (day 0) after enrollment. Measurements and Main Results: Using an unbiased gene set enrichment analysis (GSEA), we found highly divergent patterns of gene expression in AMs and PBMs. Notably, immuno-inflammatory gene sets were enriched in AM isolated on day 0 in those who survived and had more ventilator-free days (VFD); however, this association between inflammatory and immune gene sets and good outcomes was not seen in PBMs. Conclusion: Transcriptional responses during ARDS are remarkably different between AM and PBM.
2017-04-30 | GSE89953 | GEO
Project description:Transcriptome of amniotic fluid neutrophils and monocytes/macrophages
| PRJNA918599 | ENA
Project description:CD14+ monocytes sorted from the synovial fluid or peripheral blood of rheumatoid arthritis patients were analyzed by full transcriptome microarray analysis. Monocytes from healthy control samples (peripheral blood) were also profiled.
2017-01-30 | GSE71370 | GEO
Project description:Many lung diseases remain understudied due to a lack of experimental models. Lung organoids, which consist of self-organizing epithelial cells, provide versatile in vitro models for normal and abnormal biology, drug screening, gene editing, and personalized therapeutics. However, human organoids are generally derived from lung tissue, which is not commonly obtained and represents only a small fraction of lung pathologies. Induced pluripotent stem cells have provided an important alternative but require complex manipulation. Recently, one study reported airway organoids from bronchoalveolar lavage (BAL) fluid, though sample sizes and characterization were limited. Here, we demonstrate robust establishment of airway organoids from a variety of human BAL samples and show that these organoids consist predominantly of basal cells plus differentiated airway cell types including secretory, ciliated, KRT13+ “hillock,” and ionocyte cells. Furthermore, we report the development of BAL-derived alveolar organoids comprised of alveolar type 2 (AT2) cells. These techniques significantly expand the scope of lung diseases that can be studied using safely accessible primary human cells.
2024-05-01 | GSE254166 | GEO
Project description:Human Airway and Alveolar Organoids from Bronchoalveolar Lavage Fluid
| PRJNA1068661 | ENA
Project description:CD4+ T cells contribute to lung inflammation in acute respiratory distress syndrome. The CD4+ T-cell response in pediatric acute respiratory distress syndrome (PARDS) is unknown.ObjectivesTo identify differentially expressed genes and networks using a novel transcriptomic reporter assay with donor CD4+ T cells exposed to the airway fluid of intubated children with mild versus severe PARDS.DesignIn vitro pilot study.SettingLaboratory-based study using human airway fluid samples admitted to a 36-bed university-affiliated pediatric intensive care unit.Patients/subjectsSeven children with severe PARDS, nine children with mild PARDS, and four intubated children without lung injury as controls.InterventionsNone.Measurements and main resultsWe performed bulk RNA sequencing using a transcriptomic reporter assay of CD4+ T cells exposed to airway fluid from intubated children to discover gene networks differentiating severe from mild PARDS. We found that innate immunity pathways, type I (α and β), and type II (γ) interferon response and cytokine/chemokine signaling are downregulated in CD4+ T cells exposed to airway fluid from intubated children with severe PARDS compared with those with mild PARDS.ConclusionsWe identified gene networks important to the PARDS airway immune response using bulk RNA sequencing from a novel CD4+ T-cell reporter assay that exposed CD4+ T cells to airway fluid from intubated children with severe and mild PARDS. These pathways will help drive mechanistic investigations into PARDS. Validation of our findings using this transcriptomic reporter assay strategy is needed.
| S-EPMC10292738 | biostudies-literature