The authors used highly differentiated primary human 3D tissue models infected with SARS-CoV-2 patient isolates. Viral load, viral infectivity, intracellular complement activation, inflammatory mechanisms, and tissue destruction were analyzed by real-time RT-PCR, high content screening, plaque assays, luminex analyses, and transepithelial electrical resistance measurements. The authors showed that primary normal human bronchial and small airway epithelial cells respond to SARS-CoV-2 infection by an inflated local complement component 3 (C3) mobilization. They illustrated that targeting the anaphylatoxin receptors C3a receptor and C5a receptor in nonimmune respiratory cells can prevent intrinsic lung inflammation and tissue damage. This opens up a possibility for the treatment of COVID-19.
C5aR inhibition of nonimmune cells suppresses inflammation and maintains epithelial integrity in SARS-CoV-2–infected primary human airway epithelia
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