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Longitudinal multi-omics identifies responses of megakaryocytes, erythroid cells and plasmablasts as hallmarks of severe COVID-19 trajectories [methylation]

ABSTRACT: Longitudinal multi-omics identifies responses of megakaryocytes, erythroid cells and plasmablasts as hallmarks of severe COVID-19 trajectories [methylation]

PROVIDER: PRJNA679336 | ENA |

REPOSITORIES: ENA

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Longitudinal multi-omics identifies responses of megakaryocytes, erythroid cells and plasmablasts as hallmarks of severe COVID-19 trajectories

Project description:Longitudinal multi-omics identifies responses of megakaryocytes, erythroid cells and plasmablasts as hallmarks of severe COVID-19 trajectories

| PRJNA679334 | ENA

Longitudinal multi-omics identifies responses of megakaryocytes, erythroid cells and plasmablasts as hallmarks of severe COVID-19 trajectories [sequencing]

Project description:Longitudinal multi-omics identifies responses of megakaryocytes, erythroid cells and plasmablasts as hallmarks of severe COVID-19 trajectories [sequencing]

| PRJNA679331 | ENA

Longitudinal multi-omics identifies responses of megakaryocytes, erythroid cells and plasmablasts as hallmarks of severe COVID-19 trajectories [sequencing]

Project description:In order to characterise the temporal dynamics of host response during COVID-19, we performed a longitudinal multi-omics study using a two centre German cohort of 13 patients. Bulk RNA was extracted from peripheral blood sampled at up to 5 time points per patient. At each sample point, a patient’s disease trajectory, “pseudotime”, was categorised according to clinical parameters. Both, whole transcriptome and B cell receptor sequence analysis was used to determine signatures specific to different disease trajectories. We identified coexpression modules that were associated with specific patterns across different COVID-19 disease trajectories. One module identified was related to failing interferon I response at the peak of disease severity. A second module showed biphasic upregulation of transcripts associated with erythropoiesis. Bulk BCR identified expansion of IgA+ and IgG+ cells. In sum, this study demonstrated distinct gene expression dynamics upon SARS-CoV-2 infection.

2020-12-11 | GSE161777 | GEO

Longitudinal multi-omics identifies responses of megakaryocytes, erythroid cells and plasmablasts as hallmarks of severe COVID-19 trajectories

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-12-11 | GSE161778 | GEO

Longitudinal Multi-omics Analyses Identify Responses of Megakaryocytes, Erythroid Cells, and Plasmablasts as Hallmarks of Severe COVID-19.

Project description:Temporal resolution of cellular features associated with a severe COVID-19 disease trajectory is needed for understanding skewed immune responses and defining predictors of outcome. Here, we performed a longitudinal multi-omics study using a two-center cohort of 14 patients. We analyzed the bulk transcriptome, bulk DNA methylome, and single-cell transcriptome (>358,000 cells, including BCR profiles) of peripheral blood samples harvested from up to 5 time points. Validation was performed in two independent cohorts of COVID-19 patients. Severe COVID-19 was characterized by an increase of proliferating, metabolically hyperactive plasmablasts. Coinciding with critical illness, we also identified an expansion of interferon-activated circulating megakaryocytes and increased erythropoiesis with features of hypoxic signaling. Megakaryocyte- and erythroid-cell-derived co-expression modules were predictive of fatal disease outcome. The study demonstrates broad cellular effects of SARS-CoV-2 infection beyond adaptive immune cells and provides an entry point toward developing biomarkers and targeted treatments of patients with COVID-19.

| S-EPMC7689306 | biostudies-literature

Longitudinal multi-omics identifies responses of megakaryocytes, erythroid cells and plasmablasts as hallmarks of severe COVID-19 trajectories [methylation]

Project description:To help characterise the temporal dynamics of host response during COVID-19, we performed a longitudinal DNA methylation analysis in a cohort of 12 patients. DNA was extracted from peripheral blood sampled at up to 5 time points per patient. At each sample point, a patient’s disease trajectory, “pseudotime”, was categorised according to clinical parameters. DNA methylation profiling by Illumina Bead Arrays was performed on each sample. We found CpG sites hypomethylated during COVID-19 were highly enriched in cis of transcripts related to positive regulation of TNF secretion and innate immune signalling, indicating potential long-term regulation of immunological misfiring by epigenetic processes.

2020-12-11 | GSE161678 | GEO

Microarray comparison of adult peripheral blood megakaryocytes to umbilical cord blood-derived megakaryocytes

Project description:Primary adult peripheral blood (PB) megakaryocytes and umbilical cord blood (CB) megakaryocytes

2024-05-10 | GSE264384 | GEO

Longitudinal full-length IGH repertoire profiling and clonal lineage dynamics in memory B cells, plasmablasts and plasma cells of human peripheral blood

Project description:To study longitudinal dynamics of IGH BCR repertoires and clonal lineages evolution of memory B-cells, plasmablasts and plasma cells from peripheral blood of healthy donors, which were sampled three times within a year

2022-09-15 | E-MTAB-11193 | biostudies-arrayexpress

Gene expression profiles of cultured megakaryocytes

Project description:Cells obtained from adipose tissue are able to differentiate into megakaryocytes. We compared the gene expression profile of human adipose tissue derived megakaryocytes with that of megakaryocytes differentiated from human CD34 positive cord blood hematopoietic stem cells.

2021-04-05 | GSE112820 | GEO

CTCF binding in B cells and Plasmablasts

Project description:The mammalian CCCTC-binding factor (CTCF) regulates gene expression through the formation of higher order chromatin structures. Recent evidence has implicated a role for CTCF in regulating gene expression in the human MHCII locus. To investigate the role of CTCF in murine MHCII gene expression we mapped CTCF binding sites in B cells (MHCII+ cells) and Plasmablasts which are differentiated B cells that have silenced MHCII gene expression. These observations lead to the identification of differential CTCF binding during differentiation in these cell types and suggest mechanims of MHCII gene regulation. Comparison of CTCF binding in B cells and Plasmablasts in mice using ChIP-seq

2014-02-05 | E-GEOD-44637 | biostudies-arrayexpress

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