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Human FPR2/ALX receptors are highly expressed in septic patients and regulate autophagy in PMA-stimulated neutrophils |
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DOI:10.46701/APJBG.2018032018123 |
KeyWord:sepsis, FPR2/ALX, BML-111, LC3 |
Author | Institution |
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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