Abstract
SARS coronavirus 2 (SARS-CoV-2) is a novel viral pathogen that causes a clinical disease called coronavirus disease 2019 (COVID-19). Although most COVID-19 cases are asymptomatic or involve mild upper respiratory tract symptoms, a significant number of patients develop severe or critical disease. Patients with severe COVID-19 commonly present with viral pneumonia that may progress to life-threatening acute respiratory distress syndrome (ARDS). Patients with COVID-19 are also predisposed to venous and arterial thromboses that are associated with a poorer prognosis. The present study identified the emergence of a low-density inflammatory neutrophil (LDN) population expressing intermediate levels of CD16 (CD16Int) in patients with COVID-19. These cells demonstrated proinflammatory gene signatures, activated platelets, spontaneously formed neutrophil extracellular traps, and enhanced phagocytic capacity and cytokine production. Strikingly, CD16Int neutrophils were also the major immune cells within the bronchoalveolar lavage fluid, exhibiting increased CXCR3 but loss of CD44 and CD38 expression. The percentage of circulating CD16Int LDNs was associated with D-dimer, ferritin, and systemic IL-6 and TNF-α levels and changed over time with altered disease status. Our data suggest that the CD16Int LDN subset contributes to COVID-19–associated coagulopathy, systemic inflammation, and ARDS. The frequency of that LDN subset in the circulation could serve as an adjunct clinical marker to monitor disease status and progression.
Highlights
In December 2019, a novel viral pathogen, SARS coronavirus 2 (SARS-CoV-2) emerged that causes a clinical disease called coronavirus disease 2019 (COVID-19)
For the neutrophil immunophenotyping study, 10 patients were initially enrolled in the severe category, as defined by necessity of mechanical ventilation within the intensive care unit (ICU), and 21 were initially enrolled in the moderate group, as patients were admitted to the hospital but were not on mechanical ventilation
The primary finding of our study is the emergence of a subpopulation of low-density inflammatory neutrophil (LDN) in patients with COVID-19 that associates with disease severity and changes over time in parallel with changing coagulation and clinical status
Summary
In December 2019, a novel viral pathogen, SARS coronavirus 2 (SARS-CoV-2) emerged that causes a clinical disease called coronavirus disease 2019 (COVID-19). Patients with severe COVID-19 commonly develop lower respiratory tract disease due to viral pneumonia that progresses to life-threatening acute respiratory distress syndrome (ARDS) in 12% to 25% of hospitalized patients [2, 3]. Fluid accumulation in the lungs that is pathognomonic for ARDS results from a combination of virally induced lung injury and the rapid influx of immune cells to fight the infection [4]. These recruited inflammatory cells are often in a hyperactivated state associated with a phenomenon known as cytokine storm [5]. Levels of all 3 cytokines are elevated in the peripheral blood of COVID-19
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