Evolution of Blood Innate Immune Cell Phenotypes Following SARS-CoV-2 Infection in Hospitalized Patients with COVID-19

Innate immune cells appear to have an important implication in the resolution and/or the aggravation of the COVID-19 pathogenesis after infection with SARS-CoV-2. To better appreciate the role of these cells during COVID-19, changes in blood eosinophil, the neutrophil and monocyte count, and levels...

Full description

Saved in:
Bibliographic Details
Main Authors: Arnaud Dendooven, Stephane Esnault, Marie Jacob, Jacques Trauet, Emeline Delaunay, Thomas Guerrier, Amali E. Samarasinghe, Floriane Mirgot, Fanny Vuotto, Karine Faure, Julien Poissy, Marc Lambert, Myriam Labalette, Guillaume Lefèvre, Julie Demaret
Format: Article
Language:English
Published: MDPI AG 2025-07-01
Series:Cells
Subjects:
Online Access:https://www.mdpi.com/2073-4409/14/14/1093
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Innate immune cells appear to have an important implication in the resolution and/or the aggravation of the COVID-19 pathogenesis after infection with SARS-CoV-2. To better appreciate the role of these cells during COVID-19, changes in blood eosinophil, the neutrophil and monocyte count, and levels of surface protein markers have been reported. However, analyses at several timepoints of multiple surface markers on granulocytes and monocytes over a period of one month after a SARS-CoV-2 infection are missing. Therefore, in this study, we performed blood eosinophil, neutrophil, and monocyte phenotyping using a list of surface proteins and flow cytometry during a period of 30 days after the hospitalization of patients with severe SARS-CoV-2 infections. Blood cell counts were reported at seven different timepoints over the 30-day period as well as measures of multiple mediators in serum using a targeted multiplex assay approach. Our results indicate a 95% drop in the blood eosinophil count by D1, with eosinophils displaying a phenotype defined as CD69/CD63/CD125<sup>high</sup> and CCR3/CD44<sup>low</sup> during the early phases of hospitalization. Conversely, by D7 the neutrophil count increased significantly and displayed an immature, activated, and immunosuppressive phenotype (i.e., 3% of CD10/CD16<sup>low</sup> and CD10<sup>low</sup>CD177<sup>high</sup>, 6.7% of CD11b<sup>high</sup>CD62L<sup>low</sup>, and 1.6% of CD16<sup>high</sup>CD62L<sup>low</sup>), corroborated by enhanced serum proteins that are markers of neutrophil activation. Finally, our results suggest a rapid recruitment of non-classical monocytes leaving CD163/CD64<sup>high</sup> and CD32<sup>low</sup> monocytes in circulation during the very early phase. In conclusion, our study reveals potential very early roles for eosinophils and monocytes in the pathogenesis of COVID-19 with a likely reprogramming of eosinophils in the bone marrow. The exact roles of the pro-inflammatory neutrophils and the functions of the eosinophils and the monocytes, as well as these innate immune cell types, interplays need to be further investigated.
ISSN:2073-4409