tetano
Editor, Senior Moderator
Eur J Immunol
. 2022 May 2.
doi: 10.1002/eji.202149680. Online ahead of print.
Alterations of blood monocyte subset distribution and surface phenotype are linked to infection severity in COVID-19 inpatients
David Haschka[SUP] 1 [/SUP], Verena Petzer[SUP] 2 [/SUP], Francesco Robert Burkert[SUP] 1 [/SUP], Gernot Fritsche[SUP] 1 [/SUP], Sophie Wildner[SUP] 1 [/SUP], Rosa Bellmann-Weiler[SUP] 1 [/SUP], Piotr Tymoszuk[SUP] 1 3 [/SUP], Guenter Weiss[SUP] 1 [/SUP]
Affiliations
Abstract
Severe coronavirus disease 19 (COVID-19) manifests with systemic immediate pro-inflammatory innate immune activation and altered iron turnover. Iron homeostasis, differentiation, and function of myeloid leukocytes are interconnected. Therefore, we characterized the cellularity, surface marker expression and iron transporter phenotype of neutrophils and monocyte subsets in COVID-19 patients within 72 hours from hospital admission, and analyzed how these parameters relate to infection severity. Between March and November 2020, blood leukocyte samples from hospitalized COVID-19 patients (n = 48) and healthy individuals (n = 7) were analyzed by flow cytometry enabling comparative analysis of 40 features. Inflammation driven neutrophil expansion, depletion of CD16[SUP]+[/SUP] non-classical monocytes and changes in surface expression of neutrophil and monocyte CD64 and CD86 were associated with COVID-19 severity. By unsupervised self-organizing map clustering, four patterns of innate myeloid response were identified and linked to varying levels of systemic inflammation, altered cellular iron trafficking and the severity of disease. These alterations of the myeloid leukocyte compartment during acute COVID-19 may be hallmarks of inefficient viral control and immune hyper-activation and may and help at risk prediction and treatment optimization. This article is protected by copyright. All rights reserved.
Keywords: COVID-19; SARS-CoV-2; immunophenotyping; monocyte subsets; neutrophils.
. 2022 May 2.
doi: 10.1002/eji.202149680. Online ahead of print.
Alterations of blood monocyte subset distribution and surface phenotype are linked to infection severity in COVID-19 inpatients
David Haschka[SUP] 1 [/SUP], Verena Petzer[SUP] 2 [/SUP], Francesco Robert Burkert[SUP] 1 [/SUP], Gernot Fritsche[SUP] 1 [/SUP], Sophie Wildner[SUP] 1 [/SUP], Rosa Bellmann-Weiler[SUP] 1 [/SUP], Piotr Tymoszuk[SUP] 1 3 [/SUP], Guenter Weiss[SUP] 1 [/SUP]
Affiliations
- PMID: 35491910
- DOI: 10.1002/eji.202149680
Abstract
Severe coronavirus disease 19 (COVID-19) manifests with systemic immediate pro-inflammatory innate immune activation and altered iron turnover. Iron homeostasis, differentiation, and function of myeloid leukocytes are interconnected. Therefore, we characterized the cellularity, surface marker expression and iron transporter phenotype of neutrophils and monocyte subsets in COVID-19 patients within 72 hours from hospital admission, and analyzed how these parameters relate to infection severity. Between March and November 2020, blood leukocyte samples from hospitalized COVID-19 patients (n = 48) and healthy individuals (n = 7) were analyzed by flow cytometry enabling comparative analysis of 40 features. Inflammation driven neutrophil expansion, depletion of CD16[SUP]+[/SUP] non-classical monocytes and changes in surface expression of neutrophil and monocyte CD64 and CD86 were associated with COVID-19 severity. By unsupervised self-organizing map clustering, four patterns of innate myeloid response were identified and linked to varying levels of systemic inflammation, altered cellular iron trafficking and the severity of disease. These alterations of the myeloid leukocyte compartment during acute COVID-19 may be hallmarks of inefficient viral control and immune hyper-activation and may and help at risk prediction and treatment optimization. This article is protected by copyright. All rights reserved.
Keywords: COVID-19; SARS-CoV-2; immunophenotyping; monocyte subsets; neutrophils.