About: Inflammasome activation in COVID-19 patients

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An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Inflammasome activation in COVID-19 patients
Creator	Arruda, Eurico Martins, Ronaldo Zamboni, Dario Silva, Camila Alves-Filho, José Cunha, Fernando Batah, Sabrina Benatti, Maíra Bonjorno, Letícia Castro, Italo Cunha, Larissa De Lima, Mikhael Giannini, Marcela Louzada-Junior, Paulo Luppino-Assad, Rodrigo Nascimento, Daniele Pontelli, Marjorie Rodrigues, Tamara Santana, Rodrigo Siyuan, Li Veras, Flavio Vilar, Fernando Isabel, Maria Almeida, Leticia Andrade, Warrison Auxiliadora-Martins, Maria Becerra, Amanda Benatti, Maira Caetite, Diego Castro, Ricardo De 13 Oliveira, Renê De Almeida, Sergio De Barros, C De Oliveira, Fabiola De Sá, Keyla Do Amaral, Natália Fabro, Alexandre Gonçalves, Augusto Ishimoto, Adriene Kohlsdorf, Tiana Lopes, F Oliveira, Samuel Perucello, Debora Toller-5 Kawahisa, Juliana
Source	MedRxiv
abstract	Severe cases of COVID-19 are characterized by a strong inflammatory process that may ultimately lead to organ failure and patient death. The NLRP3 inflammasome is a molecular platform that promotes inflammation via cleavage and activation of key inflammatory molecules including active caspase-1 (Casp1p20), IL-1{beta} and IL-18. Although the participation of the inflammasome in COVID-19 has been highly speculated, the inflammasome activation and participation in the outcome of the disease is unknown. Here we demonstrate that the NLRP3 inflammasome is activated in response to SARS-CoV-2 infection and it is active in COVID-19, influencing the clinical outcome of the disease. Studying moderate and severe COVID-19 patients, we found active NLRP3 inflammasome in PBMCs and tissues of post-mortem patients upon autopsy. Inflammasome-derived products such as Casp1p20 and IL-18 in the sera correlated with the markers of COVID-19 severity, including IL-6 and LDH. Moreover, higher levels of IL-18 and Casp1p20 are associated with disease severity and poor clinical outcome. Our results suggest that the inflammasome is key in the pathophysiology of the disease, indicating this platform as a marker of disease severity and a potential therapeutic target for COVID-19.
has issue date	2020-08-06(xsd:dateTime)
bibo:doi	10.1101/2020.08.05.20168872
has license	medrxiv
sha1sum (hex)	eadc14ea7ad44ef6accf161a2fbb9e691ffcc6c6
schema:url	https://doi.org/10.1101/2020.08.05.20168872
resource representing a document's title	Inflammasome activation in COVID-19 patients
resource representing a document's body	covid:eadc14ea7ad44ef6accf161a2fbb9e691ffcc6c6#body_text
is schema:about of	named entity 'NLRP3' named entity 'SEVERE' named entity 'PATIENT DEATH' named entity 'STRONG' named entity 'PROCESS' named entity 'ultimately' named entity 'patient' named entity 'CD14+ cells' named entity 'inflammasome' named entity 'PBMCs' named entity 'IL-2' named entity 'antibody' named entity 'USP' named entity 'antibody' named entity 'COVID' named entity 'inflammasome' named entity 'COVID' named entity 'Caspase' named entity 'correlation' named entity 'NLRP3' named entity 'IL-18' named entity 'inflammasomes' named entity 'significant effect' named entity 'CRP' named entity 'caspase-1' named entity 'SARS-CoV-2' named entity 'IL-18' named entity 'caspase-1' named entity 'Sweden' named entity 'CRP' named entity 'caspase-1' named entity 'inflammasome' named entity 'statistically significant' named entity 'SARS-CoV-2' named entity 'clinical outcome' named entity 'supernatants' named entity 'assay' named entity 'IL-18' named entity 'IL-18' named entity 'COVID' named entity 'monocytes' named entity 'IL-6'

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