Single-cell RNA-seq of human peripheral blood mononuclear cells in COVID-19
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ABSTRACT:
PROVIDER: PRJNA720088 | ENA |
REPOSITORIES: ENA
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Project description:The COVID-19 pandemic caused by SARS-CoV-2 has reached 5.5 million deaths worldwide, causing a huge impact globally. This highly contagious viral infection produces a severe acute respiratory syndrome that includes cough, mucus, fever and pneumonia. Likewise, many hospitalized patients develop severe pneumonia associated with acute respiratory distress syndrome (ARDS), besides an exacerbated and uncontrolled systemic inflammation which in some cases induce lethal cytokine storm. Although vaccines have clearly had a beneficial effect on disease development, there is still a high percentage of patients who develop pathology related to ineffective immune system response. Therefore, a thorough understanding of the modulatory mechanisms that regulate the response to SARS-CoV-2 is crucial to find effective therapeutic alternatives. Previous studies describe the relevance of Neddylation in immune system activation further its implications in viral infection. In this context, the present study postulates Neddylation, a reversible ubiquitin-like post-translational modification of proteins and controls their stability, localization and activity, as a key regulator in the immune response against SARS-CoV-2. For the first time, we describe an increase of serum global neddylation levels of COVID-19 patients particularly associated in the early response of the infection. In addition, the results showed that overactivation of neddylation control activation, proliferation, and response of peripheral blood mononuclear cells (PBMCs) derived from COVID-19 patients. Inhibition of neddylation and subsequent avoidance of activation of PBMCs, which reduces cytokine production and proteome modulation, may therefore be a critical mechanism and an efficient therapeutic approach to immunomodulate COVID -19 patients and avoid the much-feared cytokine storm.
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Project description:There is an urgent need to better understand the pathophysiology of Coronavirus disease 2019 (COVID-19), the global pandemic caused by SARS-CoV-2 which has infected more than 3 million people worldwide. Approximately 20% of patients with COVID-19 develop severe disease and 5% require intensive care. Severe disease has been associated with changes in peripheral immune activity, including increased levels of pro-inflammatory cytokines that may be produced by a subset of inflammatory monocytes, lymphopenia, and T cell exhaustion. To elucidate pathways in peripheral immune cells that might lead to immunopathology or protective immunity in severe COVID-19, we applied single-cell RNA sequencing (scRNA-seq) to profile peripheral blood mononuclear cells (PBMCs) from 7 patients hospitalized for COVID-19 and 6 healthy controls. We identify reconfiguration of peripheral immune cell phenotype in COVID-19, including a heterogeneous interferon-stimulated gene (ISG) signature, HLA class II downregulation, and a developing neutrophil population that appears closely related to plasmablasts appearing in patients with acute respiratory failure requiring mechanical ventilation. Importantly, we found that peripheral monocytes and lymphocytes do not express substantial amounts of pro-inflammatory cytokines. Collectively, we provide a cell atlas of the peripheral immune response to severe COVID-19. Sample IDs used in the manuscript were shortened for clarity. They relate to the titles of deposited files as follows: covid_555_1: C1 A covid_555_2: C1 B covid_556: C2 covid_557: C3 covid_558: C4 covid_559: C5 covid_561: C7 HIP002: H1 HIP015: H2 HIP023: H3 HIP043: H4 HIP044: H5 HIP045: H6
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Project description:Although most SARS-CoV-2-infected individuals experience mild COVID-19, some patients suffer from severe COVID-19, which is accompanied by acute respiratory distress syndrome and systemic inflammation. To identify factors driving severe progression of COVID-19, we performed single-cell RNA-seq using peripheral blood mononuclear cells (PBMCs) obtained from healthy donors, patients with mild or severe COVID-19, and patients with severe influenza. Patients with COVID-19 exhibited hyper-inflammatory signatures across all types of cells among PBMCs, particularly upregulation of the TNF/IL-1beta-driven inflammatory response as compared to severe influenza. In classical monocytes from patients with severe COVID-19, type I IFN response co-existed with the TNF/IL-1beta-driven inflammation, and this was not seen in patients with milder COVID-19 infection. Based on this, we propose that the type I IFN response exacerbates inflammation in patients with severe COVID-19 infection.
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Project description:Red blood cells (RBC) depleted whole blood from COVID-19 patients and controls was harvested and processed in order to performed 10X single cell RNA-seq. For COVID-19 patients 2 samples 10 days a part were analyzed.
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