FPR1 and acute respiratory distress syndrome: Neutrophil hepatic recruitment was delayed but not prevented, likely as a result of system redundancy and other factors, such as cytokine and DNA binding to neutrophil receptors.[76], [77], [78], [79] As well as being fewer in number, circulating and hepatic Fpr1-/- neutrophil activation was reduced during APAP-ALI, evidenced by lower surface myeloperoxidase (MPO) and decreased CD62L shedding (Fig. 3C–J; Fig. S7D).