Formyl peptide receptor 2-lipoxin receptor (FPR2/ALX) and its agonists are well-defined mechanisms in antiinflammatory and pro-resolving response, and neutrophils actively participate in inflammation. However, FPR2/ALX expression in neutrophils and the effects of FPR2/ALX agonist in autophagy of neutrophils under inflammatory circumstances are not fully understood. In this study, flow cytometric analysis and real-time PCR were used to detect the protein and mRNA expression of FPR2/ALX in neutrophils in healthy volunteers and septic patients. The effects of FPR2/ALX agonist BML-111 alone or with pro-inflammatory stimulant in neutrophils were assessed by Western blot. The results showed that both protein and mRNA expression of FPR2/ALX in neutrophils in patients with sepsis were significantly increased compared with that in healthy subjects (P
<0.05). PMA promoted the conversion of LC3- Ⅰ to LC3- Ⅱ in neutrophils, a key marker of autophagy. BML-111 alone had no effect on autophagy in neutrophils. Nevertheless, BML-111 reduced PMA-induced LC3 processing in neutrophils. Our results indicated that FPR2/ALX expression increased in neutrophils in septic patients. FPR2/ALX agonist BML-111 reduced LC3 processing in neutrophils with pro-inflammatory stimulation. These findings demonstrated a novel effect of FPR2/ALX activation in regulating autophagy.