Abstract
Severe COVID-19 is characterized by extensive pulmonary complications, to which host immune responses are believed to play a role. As the major arm of innate immunity, neutrophils are one of the first cells recruited to the site of infection where their excessive activation can contribute to lung pathology. Low-density granulocytes (LDGs) are circulating neutrophils, whose numbers increase in some autoimmune diseases and cancer, but are poorly characterized in acute viral infections. Using flow cytometry, we detected a significant increase of LDGs in the blood of acute COVID-19 patients, compared to healthy controls. Based on their surface marker expression, COVID-19-related LDGs exhibit four different populations, which display distinctive stages of granulocytic development and most likely reflect emergency myelopoiesis. Moreover, COVID-19 LDGs show a link with an elevated recruitment and activation of neutrophils. Functional assays demonstrated the immunosuppressive capacities of these cells, which might contribute to impaired lymphocyte responses during acute disease. Taken together, our data confirms a significant granulocyte activation during COVID-19 and suggests that granulocytes of lower density play a role in disease progression.
Highlights
In December 2019, a new coronavirus disease (COVID-19), caused by a novel sarbecovirus, SARS-CoV-2, emerged in Wuhan, China and spread rapidly to the rest of the world and became a pandemic
The emergence of SARS-COV-2 and the ensuing COVID-19 disease has revealed an unprecedented need to understand the pathological mechanisms of acute respiratory infections in more detail
This study identifies a population of low-density granulocytes (LDGs) in COVID-19 patient samples, which has been poorly described in the context of acute infections so far
Summary
In December 2019, a new coronavirus disease (COVID-19), caused by a novel sarbecovirus, SARS-CoV-2, emerged in Wuhan, China and spread rapidly to the rest of the world and became a pandemic. Increased neutrophil recruitment is consistently observed in severe COVID-19 [1,3,4,5,6,7] and the neutrophil count positively correlates with disease severity, while lymphocyte numbers are depleted in patients with a poorer outcome [8]. The NLR is an independent mortality risk factor for hospitalized COVID-19 patients [3,9]. Along with this neutrophil count increase, their release of oxidant enzymes, microbicidal proteins, and chromatin in the form of neutrophil extracellular traps (NETs) is elevated [10,11,12]. Released with the purpose of containing infections, NETs can potentially worsen the patient’s inflammatory state and propagate microvascular thrombosis [13,14,15], both of which represent a major issue in COVID-19 pathology
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