The Low Expression of Fc-Gamma Receptor III (CD16) and High Expression of Fc-Gamma Receptor I (CD64) on Neutrophil Granulocytes Mark Severe COVID-19 Pneumonia

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 (rho = (-)0.72; 95% CI (-)0.92-(-)0.23; p = 0.01) and CD64 as proportional (rho = 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.

Automated summary

Hyperinflammation through neutrophil granulocytes contributes to disease severity in COVID-19 pneumonia and promotes acute lung failure. Understanding the dysregulations within the myeloid cell compartment may help to improve therapies for severe COVID-19 infection.