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Neutrophil and monocyte dysfunctional effector response towards bacterial challenge in critically-ill COVID-19 patients
Preprint
em En
| PREPRINT-BIORXIV
| ID: ppbiorxiv-406306
ABSTRACT
COVID-19 displays diverse disease severities and symptoms. Elevated inflammation mediated by hypercytokinemia induces a detrimental dysregulation of immune cells. However, there is limited understanding of how SARS-CoV-2 pathogenesis impedes innate immune signaling and function against secondary bacterial infections. We assessed the influence of COVID-19 hypercytokinemia on the functional responses of neutrophils and monocytes upon bacterial challenges from acute and corresponding recovery COVID-19 ICU patients. We show that severe hypercytokinemia in COVID-19 patients correlated with bacterial superinfections. Neutrophils and monocytes from acute COVID-19 patients showed severely impaired microbicidal capacity, reflected by abrogated ROS and MPO production as well as reduced NETs upon bacterial challenges. We observed a distinct pattern of cell surface receptor expression on both neutrophils and monocytes leading to a suppressive autocrine and paracrine signaling during bacterial challenges. Our data provide insights into the innate immune status of COVID-19 patients mediated by their hypercytokinemia and its transient effect on immune dysregulation upon subsequent bacterial infections
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Texto completo:
1
Coleções:
09-preprints
Base de dados:
PREPRINT-BIORXIV
Tipo de estudo:
Experimental_studies
Idioma:
En
Ano de publicação:
2020
Tipo de documento:
Preprint