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A monocyte/dendritic cell molecular signature of SARS-CoV2-related multisystem inflammatory syndrome in children (MIS-C) with severe myocarditis [Bulk RNAseq]

ABSTRACT: A monocyte/dendritic cell molecular signature of SARS-CoV2-related multisystem inflammatory syndrome in children (MIS-C) with severe myocarditis [Bulk RNAseq]

PROVIDER: PRJNA702763 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13748108_1.fastq.gz	Fastqsanger.gz
	SRR13748108_2.fastq.gz	Fastqsanger.gz
	SRR13737135_1.fastq.gz	Fastqsanger.gz
	SRR13737135_2.fastq.gz	Fastqsanger.gz
	SRR13737136_1.fastq.gz	Fastqsanger.gz

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A monocyte/dendritic cell molecular signature of SARS-CoV2-related multisystem inflammatory syndrome in children (MIS-C) with severe myocarditis [Bulk RNAseq]

Project description:SARS-CoV-2 infection in children is generally milder than in adults, yet a proportion of cases result in hyperinflammatory conditions often including myocarditis. To better understand these cases, we applied a multi-parametric approach to the study of blood cells of 56 children hospitalized with suspicion of SARS-CoV-2 infection. The most severe forms of MIS-C (multisystem inflammatory syndrome in children related to SARS-CoV-2), that resulted in myocarditis, were characterized by elevated levels of pro-angiogenesis cytokines and several chemokines. Single-cell transcriptomic analyses identified a unique monocyte/dendritic cell gene signature that correlated with the occurrence of myocarditis, characterized by sustained NF-kB activity, associated with decreased gene expression of NF-kB inhibitors and TNF-a signaling . We also found a weak response to type-I and type-II interferons, hyperinflammation and response to oxidative stress related to increased HIF-1a and VEGF signaling. These results provide potential for a better understanding of disease pathophysiology.

2021-07-13 | GSE167028 | GEO

A monocyte/dendritic cell molecular signature of SARS-CoV2-related multisystem inflammatory syndrome in children (MIS-C) with severe myocarditis [Single cell RNAseq]

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A monocyte/dendritic cell molecular signature of SARS-CoV2-related multisystem inflammatory syndrome in children (MIS-C) with severe myocarditis

Project description:A monocyte/dendritic cell molecular signature of SARS-CoV2-related multisystem inflammatory syndrome in children (MIS-C) with severe myocarditis

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Multisystem inflammatory syndrome in children (MIS-C) serum proteomics

Project description:While fewer cases of severe Coronavirus Disease 2019 (COVID-19) are reported globally in children, a small proportion of SARS-CoV-2 infected children develop a novel pediatric febrile entity called multisystem inflammatory syndrome in children (MIS-C) that develops 2 to 5 weeks after initial SARS-CoV-2 exposure. MIS-C primarily effects male children and children of Hispanic or black descent. MIS-C manifests as a severe and uncontrolled inflammatory response with multiorgan involvement. A hyperinflammatory state is evidenced by clinical makers of inflammation including high levels of C-reactive protein (CRP), ferritin, and D-dimers, and an increased expression of pro-inflammatory cytokines. Children often present with persistent fever, severe gastrointestinal symptoms, cardiovascular manifestations, respiratory symptoms and neurological symptoms6-11,13. Cardiovascular manifestations include hypotension, shock, cardiac dysfunction, myocarditis and pericardial effusion. In the united states, admission to the intensive care unit occurs in approximately 58% of cases. To understand disease pathogenesis of MIS-C and proteins associated with the severe form of disease we performed proteomics analysis of serum or plasma samples. We collected serum from healthy children (SARS-CoV-2 negative, n=20), mild MIS-C (non-ICU, n=5) and severe MIS-C (ICU, n = 20) patients. MIS-C definition and diagnosis was performed according to CDC guidelines. Healthy adult serum (n = 4) was also used for reference ranges quality control and we obtained plasma samples from Kawasaki Disease (KD; n=7) patients that were recruited before the Coronavirus Disease 2019 (COVID-19) pandemic.

2021-09-29 | PXD025462 | Pride

A monocyte/dendritic cell molecular signature of SARS-CoV2-related multisystem inflammatory syndrome in children (MIS-C) with severe myocarditis [Single cell RNAseq]

Project description:A monocyte/dendritic cell molecular signature of SARS-CoV2-related multisystem inflammatory syndrome in children (MIS-C) with severe myocarditis [Single cell RNAseq]

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Diagnosis of multisystem inflammatory syndrome in children (MIS-C) by a whole-blood transcriptional signature

Project description:Multisystem inflammatory syndrome in children (MIS-C) occurs in some children approximately 2-6 weeks following infection with SARS-CoV-2. Clinical symptoms are highly overlapping with Kawasaki disease (KD) and bacterial (DB) and viral (DV) infections, making diagnosis particularly challenging. Host whole blood transcriptomics can reveal specific combinations of host genes whose expression patterns can distinguish between disease groups of interest. We performed whole blood RNA-Sequencing of individuals with MIS-C, KD, bacterial and viral infections to identify a number of host genes that, when combined, could be used to diagnose MIS-C. This data contains processed data only. Raw data will be available via a controlled access archive.

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Project description:Multisystem inflammatory syndrome in Children (MIS-C) occurs in children between two and six weeks following an initial SARS-CoV-2 infection. The mechanism through which a minority of children develop the hyperinflammation characteristic of MIS-C, while others remain well, is unknown. In this study we present an in-depth assessment of the proteome of children before and after SARS-CoV-2 infection, including children with MIS-C. Reassuringly, these data show that there were minimal changes to the circulating proteome in healthy children as result of SARS-CoV2 infection and there was no evidence of continued inflammation following SARS-CoV-2 infection in children. However, activation of pro-inflammatory pathways and raised circulating markers of myocardial and vascular damage were found to be significantly associated with MIS-C. Our findings have been verified in silico using publicly available proteomic datasets and hence several promising candidate biomarker proteins for diagnosis of MIS-C are identified and described herein.

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Immune dysregulation and autoreactivity correlate with disease severity in SARS-CoV-2-associated multisystem inflammatory syndrome in children

Project description:Multisystem inflammatory syndrome in children (MIS-C) is a life-threatening post-infectious complication occurring unpredictably weeks after mild or asymptomatic SARS-CoV2 infection in otherwise healthy children. Here, we define immune abnormalities in MIS-C compared to adult COVID-19 and pediatric/adult healthy controls using single-cell RNA sequencing, antigen receptor repertoire analysis, unbiased serum proteomics, and in vitro assays. Despite no evidence of active infection, we uncover elevated S100A-family alarmins in myeloid cells and marked enrichment of serum proteins that map to myeloid cells and pathways including cytokines, complement/coagulation, and fluid shear stress in MIS-C patients. Moreover, NK and CD8 T cell cytotoxicity genes are elevated, and plasmablasts harboring IgG1 and IgG3 are expanded. Consistently, we detect elevated binding of serum IgG from severe MIS-C patients to activated human cardiac microvascular endothelial cells in culture. Thus, we define immunopathology features of MIS-C with implications for predicting and managing this SARS-CoV2-induced critical illness in children.

2021-04-02 | GSE166489 | GEO

Notch1-CD22-Dependent Immune Dysregulation in the SARS-CoV2-Associated Multisystem Inflammatory Syndrome in Children

Project description:Multisystem inflammatory syndrome in children (MIS-C) evolves in some pediatric patients following acute infection with SARS-CoV-2 by hitherto unknown mechanisms. Whereas acute-COVID-19 severity and outcome were previously correlated with Notch4 expression on regulatory T (Treg) cells, here we show that the Treg cells in MIS-C additionally upregulated Notch1 expression. Genetic analysis revealed that MIS-C patients were enriched in rare deleterious variant impacting inflammation and autoimmunity pathways. Several variants mapped to Notch signaling-related genes including a loss of function mutation in the negative Notch1 regulator NUMB . Notch1 signaling in Treg cells induced CD22, leading to their destabilization in an mTORC1 dependent manner and to the promotion of systemic inflammation in proxy mouse models. These results establish the Notch1-CD22 axis as an immune dysregulatory mechanism critically involved in MIS-C and point to distinct immune checkpoints controlled by individual Treg cell Notch receptors that shape the inflammatory outcome in SARS-CoV-2 infection.

2021-12-01 | GSE186799 | GEO

A monocyte/dendritic cell molecular signature of SARS-CoV2-related multisystem inflammatory syndrome in children (MIS-C) with severe myocarditis

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

2021-07-13 | GSE167030 | GEO