The Role of NETosis and Complement Activation in COVID-19-Associated Coagulopathies

Inflammation-induced coagulopathy is a common complication associated with coronavirus disease 2019 (COVID-19). We aim to evaluate the association of NETosis and complement markers with each other as well as their association with thrombogenicity and disease severity in COVID-19. The study included...

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Published in:	Biomedicines Vol. 11; no. 5; p. 1371
Main Authors:	Ghanbari, Emily Parissa, Jakobs, Kai, Puccini, Marianna, Reinshagen, Leander, Friebel, Julian, Haghikia, Arash, Kränkel, Nicolle, Landmesser, Ulf, Rauch-Kröhnert, Ursula
Format:	Journal Article
Language:	English
Published:	Switzerland MDPI AG 05-05-2023 MDPI
Subjects:	Blood clots Blood platelets Chronic obstructive pulmonary disease Coagulation complement Complement activation Complement component C3 Complement component C5 Coronaviruses COVID-19 Diseases Health aspects Hospital patients Infections Infectious diseases Inflammation Lung diseases Lung diseases, Obstructive Medical research Medicine, Experimental NETosis Neutrophils Pathogens Patients Platelets Pneumonia Proteins Severe acute respiratory syndrome Severe acute respiratory syndrome coronavirus 2 Thromboembolism Thrombosis Viral infections United States > US Switzerland COVID-19 NETosis complement coagulation
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Summary:	Inflammation-induced coagulopathy is a common complication associated with coronavirus disease 2019 (COVID-19). We aim to evaluate the association of NETosis and complement markers with each other as well as their association with thrombogenicity and disease severity in COVID-19. The study included hospitalized patients with an acute respiratory infection: patients with SARS-CoV2 infection (COVpos, = 47) or either pneumonia or infection-triggered acute exacerbated COPD (COVneg, = 36). Our results show that NETosis, coagulation, and platelets, as well as complement markers, were significantly increased in COVpos patients, especially in severely ill COVpos patients. NETosis marker MPO/DNA complexes correlated with coagulation, platelet, and complement markers only in COVpos. Severely ill COVpos patients showed an association between complement C3 and SOFA (R = 0.48; ≤ 0.028), C5 and SOFA (R = 0.46; ≤ 0.038), and C5b-9 and SOFA (R = 0.44; ≤ 0.046). This study provides further evidence that NETosis and the complement system are key players in COVID-19 inflammation and clinical severity. Unlike previous studies that found NETosis and complement markers to be elevated in COVID-19 patients compared to healthy controls, our findings show that this characteristic distinguishes COVID-19 from other pulmonary infectious diseases. Based on our results, we propose that COVID-19 patients at high risk for immunothrombosis could be identified via elevated complement markers such as C5.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	2227-9059 2227-9059
DOI:	10.3390/biomedicines11051371