Human FPR2/ALX receptors are highly expressed in septic patients and regulate autophagy in PMA-stimulated neutrophils
  
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DOI:
KeyWord:sepsis, FPR2/ALX, BML-111, LC3
                    
AuthorInstitution
Yao Lu Department of Blood Transfusion, Research Institute of Surgery, Daping Hospital, Army Medical University, Chongqing 400042, China
Han Zhang Department of Blood Transfusion, Research Institute of Surgery, Daping Hospital, Army Medical University, Chongqing 400042, China
Wenjun Xia Department of Blood Transfusion, Research Institute of Surgery, Daping Hospital, Army Medical University, Chongqing 400042, China
Guixiang Sun Department of Blood Transfusion, Research Institute of Surgery, Daping Hospital, Army Medical University, Chongqing 400042, China
Lingfeng Wang Department of Blood Transfusion, Research Institute of Surgery, Daping Hospital, Army Medical University, Chongqing 400042, China
Linjing Zhang Department of Blood Transfusion, Research Institute of Surgery, Daping Hospital, Army Medical University, Chongqing 400042, China
Aiqing Wen Department of Blood Transfusion, Research Institute of Surgery, Daping Hospital, Army Medical University, Chongqing 400042, China
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Abstract:
      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.
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