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ABSTRACT: Metagenome assembly of PRJNA735193 data set (Oral Microbiome associated with Coronavirus disease 2019 (COVID-19))

PROVIDER: PRJEB87718 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR14736652_cleaned.contigs.fa.gz	Other
	SRR14736653_cleaned.contigs.fa.gz	Other
	SRR14736655_cleaned.contigs.fa.gz	Other
	SRR14736658_cleaned.contigs.fa.gz	Other

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Project description:Oral Microbiome associated with Coronavirus disease 2019 (COVID-19)

| PRJNA735193 | ENA

Gene expression profile at single cell level of stromal vascular cells (SVC) from the subcutaneous adipose tissue (SAT) and the visceral adipose tissue (VAT) post-exposure to SARS-CoV-2 or mock conditions in vitro

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Small RNA-seq analysis of serum miRNAs in patients with severe COVID-19

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High titers and low fucosylation of early anti-SARS-CoV-2 IgG promote hyper-inflammation by anti-inflammatory macrophages (MIL10)

Project description:Patients diagnosed with coronavirus disease 2019 (COVID-19) mostly become critically ill around the time of activation of the adaptive immune response. Here, we provide evidence that antibodies play a role in the worsening of disease at the time of seroconversion. We show that early phase severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2) spike protein-specific IgG in serum of critically ill COVID-19 patients induces hyper-inflammatory responses by human alveolar macrophages. We identified that this excessive inflammatory response is dependent on two antibody features that are specific for patients with severe COVID-19. First, inflammation is driven by high titers of anti-spike IgG, a hallmark of severe disease. Second, we found that anti-spike IgG from patients with severe COVID-19 is intrinsically more pro-inflammatory because of different glycosylation, particularly low fucosylation, of the Fc tail. Notably, low anti-spike IgG fucosylation normalized in a few weeks after initial infection with SARS-CoV-2, indicating that the increased antibody-dependent inflammation mainly occurs at the time of seroconversion. We identified Fcγ Receptor (FcγR) IIa and FcγRIII as the two primary IgG receptors that are responsible for the induction of key COVID-19-associated cytokines such as interleukin-6 and tumor necrosis factor. In addition, we show that anti-spike IgG-activated macrophages can subsequently break pulmonary endothelial barrier integrity and induce microvascular thrombosis in vitro. Finally, we demonstrate that the hyper-inflammatory response induced by anti-spike IgG can be specifically counteracted by fostamatinib, an FDA- and EMA-approved therapeutic small molecule inhibitor of the kinase, Syk.

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Type 2 inflammation reduces SARS-CoV-2 replication in the airway epithelium in allergic asthma through functional alteration of ciliated epithelial cells II

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