Innate Immunity and Inflammasome activation in response to SARS-CoV-2

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Global Immunotalks

Virtual seminars in immunology. Launched by Carla Rothlin and Elina Zúñiga @ZunigaLab

Field of Study: Biology , Published 17 Projects

Tuberculosis Infection IgA animal model COVID-19

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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-1β 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.

NLRP3
NLRP3 1 Project
COVID-19
COVID-19 19 Projects
Coronavirus
Coronavirus 5 Projects
Immunology
Immunology 27 Projects
Inflammasome
Inflammasome 1 Project
SARS-CoV-2
SARS-CoV-2 17 Projects