NLRP3 and bacterial infectious disease: These findings show that even though SARS-CoV-2 can only infect lung epithelial cells in K18-hACE-2 mice, it also activates NLRP3 inflammatory signaling resulting in the release of cytokine IL-1β, which may suppress VE-cadherin in neighboring noninfected endothelial cells, mirroring what has been reported for VE-cadherin downregulation in bacterial infections.17