Hyperinflammation through neutrophil granulocytes contributes to disease severity in COVID-19 pneumonia and promotes acute lung failure. Understanding the mechanisms of the dysregulations within the myeloid cell compartment may help to… Click to show full abstract
Hyperinflammation through neutrophil granulocytes contributes to disease severity in COVID-19 pneumonia and promotes acute lung failure. Understanding the mechanisms of the dysregulations within the myeloid cell compartment may help to improve therapies for severe COVID-19 infection. Here, we investigated the immunopathological characteristics of circulating neutrophil granulocytes and monocytes in 16 patients with COVID-19 pneumonia by multiparameter flow cytometry in comparison to 9 patients with pulmonary infiltrates but without COVID-19. We correlated the immunophenotypes with the scores of the severity-of-disease classification system, APACHE-II. We found that the mean fluorescence intensity (MFI) of CD15, which is important for the transendothelial migration, was significantly reduced in the patients with COVID-19 (difference ± SD; 295.70 ± 117.50 MFI; p = 0.02). In addition, the granularity was significantly lower in the neutrophil granulocytes of patients with COVID-19 (difference ± SD; 1.11 ± 0.43 side-scatter ratio; p = 0.02). Moreover, the Fc-gamma receptor III (CD16) and Fc-gamma receptor I (CD64) on the neutrophil granulocytes were expressed discordantly with COVID-19 severity. CD16 correlated as inversely proportional (ρ = (−)0.72; 95% CI (−)0.92–(−)0.23; p = 0.01) and CD64 as proportional (ρ = 0.76; 95% CI 0.31–0.93; p = 0.01) with the APACHE-II scores of the patients. We conclude that the deviant expression of the Fc-gamma receptors might play role in a dysregulated antibody-mediated phagocytosis in severe cases of COVID-19 pneumonia.
               
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