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RNAseq analysis of blood from patients with Multisystem Inflammatory Syndrome in Children (MISC)

ABSTRACT: RNAseq analysis of blood from patients with Multisystem Inflammatory Syndrome in Children (MISC)

PROVIDER: PRJNA746233 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15116400_1.fastq.gz	Fastqsanger.gz
	SRR15116400_2.fastq.gz	Fastqsanger.gz
	SRR15116401_1.fastq.gz	Fastqsanger.gz
	SRR15116401_2.fastq.gz	Fastqsanger.gz
	SRR15116402_1.fastq.gz	Fastqsanger.gz

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

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Project description:During the COVID-19 pandemic, Multisystem Inflammatory Syndrome in Children (MIS-C) emerged as a disease with unknown causes and no specific diagnostic test. We used artificial intelligence in a nationwide study from April 2020 to March 2022 to identify a 4-protein diagnostic signature for MIS-C. This signature had an AUC of 1.0 for distinguishing MIS-C from other febrile diseases. Our analysis also revealed intricate protein patterns, indicating that MIS-C is associated with immune dysregulation, lipid metabolism changes, increased coagulation activity, and tissue remodeling.

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Project description:Multisystem Inflammatory Syndrome in Children (MIS-C) is a delayed-onset, COVID-19-related hyperinflammatory illness characterized by SARS-CoV-2 antigenemia, cytokine storm, and immune dysregulation. In severe COVID-19, neutrophil activation is central to hyperinflammatory complications, yet the role of neutrophils in MIS-C is undefined. Here, we collect blood from 152 children: 31 cases of MIS-C, 43 cases of acute pediatric COVID-19, and 78 pediatric controls. We find that MIS-C neutrophils display a granulocytic myeloid-derived suppressor cell (G-MDSC) signature with highly altered metabolism, distinct from the neutrophil interferon-stimulated gene (ISG) response we observe in pediatric COVID-19. Moreover, we observe extensive spontaneous neutrophil extracellular trap (NET) formation in MIS-C, and we identify neutrophil activation and degranulation signatures. Mechanistically, we determine that SARS-CoV-2 immune complexes are sufficient to trigger NETosis. Our findings suggest that the hyperinflammatory presentation during MIS-C could be mechanistically linked to persistent SARS-CoV-2 antigenemia, driven by uncontrolled neutrophil activation and NET release in the vasculature.

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

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