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Elevated Myl9 reflects the Myl9-containing microthrombi in SARS-CoV-2-induced exudative vasculitis and predicts COVID-19 severity

ABSTRACT: Elevated Myl9 reflects the Myl9-containing microthrombi in SARS-CoV-2-induced exudative vasculitis and predicts COVID-19 severity

PROVIDER: PRJNA859437 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20277800_1.fastq.gz	Fastqsanger.gz
	SRR20277800_2.fastq.gz	Fastqsanger.gz
	SRR20277900_1.fastq.gz	Fastqsanger.gz
	SRR20277900_2.fastq.gz	Fastqsanger.gz
	SRR20277801_1.fastq.gz	Fastqsanger.gz

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Elevated Myl9 reflects the Myl9-containing microthrombi in SARS-CoV-2-induced exudative vasculitis and predicts COVID-19 severity

Project description:The mortality of coronavirus disease 2019 (COVID-19) is strongly correlated with pulmonary vascular pathology accompanied by SARS-CoV-2 infection-triggered immune dysregulation and aberrant activation of platelets. We combined histological analyses using field emission scanning electron microscopy with energy-dispersive X-ray spectroscopy analyses of the lungs from autopsy samples and single-cell RNA sequencing of peripheral blood mononuclear cells to investigate the pathogenesis of vasculitis and immunothrombosis in COVID-19. We found that SARS-CoV-2 accumulated in the pulmonary vessels, causing exudative vasculitis accompanied by the emergence of thrombospondin-1 (THBS-1)-expressing non-canonical monocytes and the formation of Myosin light chain 9 (Myl9)-containing microthrombi in the lung of COVID-19 patients with fatal disease. The amount of plasma Myl9 in COVID-19 was correlated with the clinical severity and measuring plasma Myl9 together with other markers allowed us to predict the severity of the disease more accurately. This study provides detailed insight into the pathogenesis of vasculitis and immunothrombosis, which may lead to optimal medical treatment for COVID-19.

2022-07-21 | GSE208337 | GEO

Elevated Myl9 reflects the Myl9-containing microthrombi in SARS-CoV-2-induced lung exudative vasculitis and predicts COVID-19 severity.

Project description:The mortality of coronavirus disease 2019 (COVID-19) is strongly correlated with pulmonary vascular pathology accompanied by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection-triggered immune dysregulation and aberrant activation of platelets. We combined histological analyses using field emission scanning electron microscopy with energy-dispersive X-ray spectroscopy analyses of the lungs from autopsy samples and single-cell RNA sequencing of peripheral blood mononuclear cells to investigate the pathogenesis of vasculitis and immunothrombosis in COVID-19. We found that SARS-CoV-2 accumulated in the pulmonary vessels, causing exudative vasculitis accompanied by the emergence of thrombospondin-1-expressing noncanonical monocytes and the formation of myosin light chain 9 (Myl9)-containing microthrombi in the lung of COVID-19 patients with fatal disease. The amount of plasma Myl9 in COVID-19 was correlated with the clinical severity, and measuring plasma Myl9 together with other markers allowed us to predict the severity of the disease more accurately. This study provides detailed insight into the pathogenesis of vasculitis and immunothrombosis, which may lead to optimal medical treatment for COVID-19.

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Project description:Purpose: The goal of this study was to compare gene expression profiles from whole blood RNA-Seq data from pediatric ANCA-associated vasculitis patients to identify mechanistic endotypes. Methods: Whole blood mRNA profiles were generated from pediatric and adult vasculitis patients using Illumina GAIIx or Hi Seq 2500 RNA-Seq. Fastq files were alinged to human genome version GRC38.91 using STAR v2.6 and count data was generated with HTSEQ v0.61p1. Counts that passed quality and minimum expression filteres were anlayzed by hierarchical clustering based on Euclidean distance, and then for differential expression with DESeq2. Results: Our workflow identified 14,156 transcripts consistently expressed in vasculitis patients. Distance hierarchcial clustering identified three groups within these pediatric samples, and two groups plus one outlier in the adult samples. The two largest pediatric clusters were used as groups for differential expression analysis with the DESeq2 package for R. DE analysis identified 3,809 differentially expressed genes between clusters. Between the two adult groups, 1,682 genes were differentially expressed. DE genes were anlayzed for enrichment using ReatomePA as the reference database. This analysis revealed that genes involved in T-cell mediated immunity are more highly expressed in pediatric patients that fell into one endotype and those involved in neutrophil and Toll-like receptor mediated inflammation are more highly expressed in pediatric patients that fell into the other endotype group. Similar results were also seen in adults. Conclusions: This study utilizes RNA-Seq data to investigate the etiologies of ANCA-associated vasculitis. Using this approach we have identified T-cell mediated immunity and Toll-like receptor mediated inflammation as potentially differing inflammatory mechanisms in both pediatric and adult vasculitis patients that do not fall along normal diagnostic criteria.

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