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Monocyte-driven atypical cytokine storm and aberrant neutrophil activation as key mediators of COVID-19 disease severity

Vanderbeke, L ; Van Mol, P ; Van Herck, Y ; De Smet, F ; Humblet-Baron, S ; Martinod, K ; Antoranz, A ; Arijs, I ; Boeckx, B ; Bosisio, F M ; Casaer, M ; Dauwe, D ; De Wever, W ; Dooms, C ; Dreesen, E ; Emmaneel, A ; Filtjens, J ; Gouwy, M ; Gunst, J ; Hermans, G ; Jansen, S ; Lagrou, K ; Liston, A ; Lorent, N ; Meersseman, P ; Mercier, T ; Neyts, J ; Odent, J ; Panovska, D ; Penttila, P A ; Pollet, E ; Proost, P ; Qian, J ; Quintelier, K ; Raes, J ; Rex, S ; Saeys, Y ; Sprooten, J ; Tejpar, S ; Testelmans, D ; Thevissen, K ; Van Buyten, T ; Vandenhaute, J ; Van Gassen, S ; Velásquez Pereira, L C ; Vos, R ; Weynand, B ; Wilmer, A ; Yserbyt, J ; Garg, A D ; Matthys, P ; Wouters, C ; Lambrechts, D ; Wauters, E ; Wauters, J

Nature communications, 2021-07, Vol.12 (1), p.4117-4117, Article 4117 [Periódico revisado por pares]

England: Nature Publishing Group

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Título:
Monocyte-driven atypical cytokine storm and aberrant neutrophil activation as key mediators of COVID-19 disease severity
Autor: Vanderbeke, L ; Van Mol, P ; Van Herck, Y ; De Smet, F ; Humblet-Baron, S ; Martinod, K ; Antoranz, A ; Arijs, I ; Boeckx, B ; Bosisio, F M ; Casaer, M ; Dauwe, D ; De Wever, W ; Dooms, C ; Dreesen, E ; Emmaneel, A ; Filtjens, J ; Gouwy, M ; Gunst, J ; Hermans, G ; Jansen, S ; Lagrou, K ; Liston, A ; Lorent, N ; Meersseman, P ; Mercier, T ; Neyts, J ; Odent, J ; Panovska, D ; Penttila, P A ; Pollet, E ; Proost, P ; Qian, J ; Quintelier, K ; Raes, J ; Rex, S ; Saeys, Y ; Sprooten, J ; Tejpar, S ; Testelmans, D ; Thevissen, K ; Van Buyten, T ; Vandenhaute, J ; Van Gassen, S ; Velásquez Pereira, L C ; Vos, R ; Weynand, B ; Wilmer, A ; Yserbyt, J ; Garg, A D ; Matthys, P ; Wouters, C ; Lambrechts, D ; Wauters, E ; Wauters, J
Assuntos: Adaptive systems ; Aged ; Antigen-Presenting Cells - immunology ; Antigens ; Case-Control Studies ; CD8 antigen ; Cell activation ; Coronaviruses ; COVID-19 ; COVID-19 - blood ; COVID-19 - complications ; COVID-19 - immunology ; COVID-19 - virology ; Cytokine Release Syndrome - blood ; Cytokine Release Syndrome - complications ; Cytokine Release Syndrome - pathology ; Cytokine Release Syndrome - virology ; Cytokine storm ; Cytokines ; Cytokines - blood ; Damage ; Depth profiling ; Epidemiology ; Extracellular Traps - metabolism ; Female ; Histocompatibility Antigens Class II - metabolism ; Humans ; Immune response ; Immune system ; Immunophenotyping ; Inflammation ; Interferon ; Leukocytes (neutrophilic) ; Lymphocytes ; Lymphocytes T ; Macrophages ; Male ; Middle Aged ; Monocytes ; Monocytes - pathology ; Neutrophil Activation ; Neutrophils ; Phenotypes ; SARS-CoV-2 - physiology ; Severe acute respiratory syndrome ; Severe acute respiratory syndrome coronavirus 2 ; Severity of Illness Index ; Viral diseases ; Virulence ; Viruses ; γ-Interferon
É parte de: Nature communications, 2021-07, Vol.12 (1), p.4117-4117, Article 4117
Notas: ObjectType-Article-1
SourceType-Scholarly Journals-1
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Descrição: Epidemiological and clinical reports indicate that SARS-CoV-2 virulence hinges upon the triggering of an aberrant host immune response, more so than on direct virus-induced cellular damage. To elucidate the immunopathology underlying COVID-19 severity, we perform cytokine and multiplex immune profiling in COVID-19 patients. We show that hypercytokinemia in COVID-19 differs from the interferon-gamma-driven cytokine storm in macrophage activation syndrome, and is more pronounced in critical versus mild-moderate COVID-19. Systems modelling of cytokine levels paired with deep-immune profiling shows that classical monocytes drive this hyper-inflammatory phenotype and that a reduction in T-lymphocytes correlates with disease severity, with CD8+ cells being disproportionately affected. Antigen presenting machinery expression is also reduced in critical disease. Furthermore, we report that neutrophils contribute to disease severity and local tissue damage by amplification of hypercytokinemia and the formation of neutrophil extracellular traps. Together our findings suggest a myeloid-driven immunopathology, in which hyperactivated neutrophils and an ineffective adaptive immune system act as mediators of COVID-19 disease severity.
Editor: England: Nature Publishing Group
Idioma: Inglês

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Monocyte-driven atypical cytokine storm and aberrant neutrophil activation as key mediators of COVID-19 disease severity

England: Nature Publishing Group

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