TLR4 and acute respiratory distress syndrome: SARS-CoV-2 is hypothesized to directly bind the primary PRR for LPS, Toll-like receptors 4 (TLR4), and activate TLR4 signaling to enhance ACE2 expression on the alveocyte surface, enabling SARS-CoV-2 penetration and contributing to the development of ARDS [90].