Therefore, we developed a monoclonal anti-TLR4 antibody (ATAB) in our lab that can bind to TLR4 with a high affinity and inhibit LPS-induced TLR4 signaling (29), and we hypothesized that ATAB may have a therapeutic effect on APAP-induced ALI and that the gut microbiota may mediate this effect. Here, TLR4 is linked to acute respiratory distress syndrome.