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Fig. 4 | Respiratory Research

Fig. 4

From: Pulmonary vascular inflammation with fatal coronavirus disease 2019 (COVID-19): possible role for the NLRP3 inflammasome

Fig. 4

A ARDS (and mechanical ventilation) associated with COVID-19 seems to be largely responsible for activation of the NLRP3 inflammasome. This pathway seems to be ARDS related and not COVID-19 (SARS CoV2 virus infection) specific. B Overview of SARS-CoV-2 entry, infection and endothelial inflammation and cell death. As is well established, oral nasopharyngeal entry of SARS-CoV-2 is followed by its binding to the alveolar epithelium. The infected pneumocytes secrete cytokine and chemokines, which attract neutrophils to the alveolar space, leading to a possible breach of the alveolar wall. Meanwhile, endothelial cells overexpress NLRP3 as we observed in the autopsies (either by infection, or via increased amounts of chemokines and cytokines). The NLRP3 pathway drives endothelial pyroptosis. This leads to breakdown of the endothelial-alveolar barrier and causes interstitial and alveolar space flooding. Endothelial cell death and debris activate coagulation cascades that promotes thrombi formation

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