About: Complement and tissue factor-enriched neutrophil extracellular traps are key drivers in COVID-19 immunothrombosis

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About: Complement and tissue factor-enriched neutrophil extracellular traps are key drivers in COVID-19 immunothrombosis Goto Sponge NotDistinct Permalink

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Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Complement and tissue factor-enriched neutrophil extracellular traps are key drivers in COVID-19 immunothrombosis
Creator	Ritis, Konstantinos Lambris, John Tsigalou, Christina Chrysanthopoulou, Akrivi Germanidis, Georgios Konstantinidis, Theocharis Mastellos, Dimitrios Metallidis, Simeon Mitroulis, Ioannis Mitsios, Alexandros Ntinopoulou, Maria Papagoras, Charalampos Rafailidis, Petros Sertaridou, Eleni Skendros, Panagiotis Tektonidou, Maria Tsironidou, Victoria
Source	MedRxiv
abstract	Emerging data indicate that complement and neutrophils are involved in the maladaptive host immune response that fuels hyper-inflammation and thrombotic microangiopathy increasing the mortality rate in coronavirus disease 2019 (COVID-19). Here, we investigated the interaction between complement and the platelet/neutrophil extracellular traps (NETs)/thrombin axis, using COVID-19 clinical samples, cell-based inhibition studies and NETs/human aortic endothelial cell (HAEC) co-cultures. Increased plasma levels of NETs, TF activity and sC5b-9 were detected in patients. Neutrophils yielded high tissue factor (TF) expression and released NETs carrying functionally active TF. Confirming our ex vivo findings, treatment of control neutrophils with COVID-19 platelet-rich plasma generated TF-bearing NETs that induced thrombotic activity of HAEC. Thrombin or NETosis inhibition or C5aR1 blockade attenuated platelet-mediated NET-driven thrombogenicity. Serum isolated from COVID-19 patients induces complement activation in vitro, which is consistent with high complement activity in clinical samples. Complement inhibition at the level of C3 with compstatin Cp40 disrupted TF expression in neutrophils. In conclusion, we provide a mechanistic basis that reveals the pivotal role of complement and NETs in COVID-19 immmunothrombosis. This study supports emerging strategies against SARS-CoV-2 infection that exploit complement therapeutics or NETosis inhibition.
has issue date	2020-06-16(xsd:dateTime)
bibo:doi	10.1101/2020.06.15.20131029
has license	medrxiv
sha1sum (hex)	60a51b253e701aa6705e1975893e841688647a48
schema:url	https://doi.org/10.1101/2020.06.15.20131029
resource representing a document's title	Complement and tissue factor-enriched neutrophil extracellular traps are key drivers in COVID-19 immunothrombosis
resource representing a document's body	covid:60a51b253e701aa6705e1975893e841688647a48#body_text
is schema:about of	named entity 'APL' named entity 'inventor' named entity 'neutrophil extracellular traps' named entity 'COVID-19' named entity 'PEGylated' named entity 'JDL' named entity 'therapeutic purposes' named entity 'JDL' named entity 'therapeutic purposes' named entity 'tissue factor' named entity 'thrombin' named entity 'Declaration of Helsinki' named entity 'NETs' named entity 'coagulopathy' named entity 'medRxiv' named entity 'immune complexes' named entity 'neutrophils' named entity 'pathological process' named entity 'neutrophils' named entity 'platelet' named entity 'immune response' named entity 'serum' named entity 'PRP' named entity 'thrombin' named entity 'COVID-19' named entity 'neutrophils' named entity 'neutrophil elastase' named entity 'COVID' named entity 'platelet' named entity 'measure the levels' named entity 'autophagy' named entity 'medRxiv' named entity 'COVID' named entity 'CC-BY-NC-ND 4.0' named entity 'therapeutic targets' named entity 'C5a' named entity 'Serum' named entity 'common cold' named entity 'COVID' named entity 'neutrophils' named entity 'C5a' named entity 'COVID-19' named entity 'severe acute respiratory syndrome coronavirus 2' named entity 'medRxiv' named entity 'severe acute respiratory syndrome coronavirus 2' named entity 'medRxiv' named entity 'PRP' named entity 'inflammatory response' named entity 'NETosis' named entity 'neutrophils' named entity 'SARS-CoV-2 virus' named entity 'autophagy' named entity 'C5a' named entity 'complement' named entity 'thrombogenicity' named entity 'neutrophil' named entity 'neutrophils' named entity 'mRNA' named entity 'COVID-19' named entity 'complement' named entity 'thrombotic microangiopathy' named entity 'inflammatory disorders' named entity 'complement' named entity 'COVID-19' named entity 'HCQ' named entity 'immunofluorescence microscopy' named entity 'immunocomplexes' named entity 'qPCR' named entity 'vicious cycle'

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