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.