Amanda Becerra

TL;DR: This work shows that inflammasomes are activated in response to SARS-CoV-2 infection in vitro and in COVID-19 patients, contributing to the exacerbated inflammatory response, impacting disease progression and clinical outcome.

TL;DR: It is demonstrated 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.

TL;DR: The findings reveal that dysfunctional efferocytosis of SARS-CoV-2-infected cell corpses suppresses macrophage anti-inflammation and efficient tissue repair programs and provides mechanistic insights for the excessive production of pro-inflammatory cytokines and accumulation of tissue damage associated with COVID-19 immunopathogenesis.

TL;DR: A high-throughput screening using a 2560 small-molecule compound library and identified FDA-approved drugs that function as pan-inflammasome inhibitors is performed and niclosamide (NIC) is identified as the best hit, effectively inhibits both inflammaome activation and SARS-CoV-2 replication.

TL;DR: In this article, the authors show that engulfment of SARS-CoV2-infected apoptotic cells (AC) exacerbates inflammatory cytokine production, inhibits the expression of efferocytic receptors, and impairs continual efferocytetosis by macrophages.