留言板

尊敬的读者、作者、审稿人, 关于本刊的投稿、审稿、编辑和出版的任何问题, 您可以本页添加留言。我们将尽快给您答复。谢谢您的支持!

姓名
邮箱
手机号码
标题
留言内容
验证码

协调组织修复:控制有害和修复性中性粒细胞功能的分子途径

贺伟峰 闫凌峰

贺伟峰, 闫凌峰. 协调组织修复:控制有害和修复性中性粒细胞功能的分子途径[J]. 中华烧伤与创面修复杂志, 2024, 40(5): 1-8. DOI: 10.3760/cma.j.cn501225-20240306-00089.
引用本文: 贺伟峰, 闫凌峰. 协调组织修复:控制有害和修复性中性粒细胞功能的分子途径[J]. 中华烧伤与创面修复杂志, 2024, 40(5): 1-8. DOI: 10.3760/cma.j.cn501225-20240306-00089.
He Weifeng,Yan Lingfeng.Coordinating tissue repair: molecular pathways controlling the function of harmful and repairing neutrophils[J].Chin J Burns Wounds,2024,40(5):1-8.DOI: 10.3760/cma.j.cn501225-20240306-00089.
Citation: He Weifeng,Yan Lingfeng.Coordinating tissue repair: molecular pathways controlling the function of harmful and repairing neutrophils[J].Chin J Burns Wounds,2024,40(5):1-8.DOI: 10.3760/cma.j.cn501225-20240306-00089.

协调组织修复:控制有害和修复性中性粒细胞功能的分子途径

doi: 10.3760/cma.j.cn501225-20240306-00089
基金项目: 

国家自然科学基金面上项目 31872742, 82172232

军队医学科技青年培育计划 20QNPY024

陆军军医大学科技创新能力提升专项 2019XQY12

详细信息
    通讯作者:

    贺伟峰,Email:whe761211@hotmail.com

Coordinating tissue repair: molecular pathways controlling the function of harmful and repairing neutrophils

Funds: 

General Program of National Natural Science Foundation of China 31872742, 82172232

Military Medical Science and Technology Youth Training Program 20QNPY024

Special Project for Enhancing Science and Technology Innovation Ability of Army Medical University 2019XQY12

More Information
  • 摘要: 中性粒细胞是最丰富的循环白细胞,作为损伤组织和感染部位的第一反应者,在愈合早期炎症反应中起着不可或缺的作用。中性粒细胞通过吞噬和破坏病原体、释放细胞毒性酶和代谢物以及传播炎症网络来提供即时宿主防御。然而,如果不加以控制,这些防御机制会造成重大的附带损害。专注于有害中性粒细胞炎症的诱因和免疫调节缺陷,并把握有害炎症的特定驱动因素,对重新校准炎症以促进内源性组织修复具有重要意义。该文从中性粒细胞炎症失衡的诱因出发,阐述中性粒细胞介导组织损伤的主要机制及相关病理表现,并强调了具有应用前景的治疗靶点。

     

  • [1] 孙炳伟,黄佳敏.中性粒细胞生理与病理生理作用再认识[J].中华烧伤与创面修复杂志,2022,38(2):109-113.DOI: 10.3760/cma.j.cn501120-20211122-00391.
    [2] LiuY,XiangC,QueZ,et al.Neutrophil heterogeneity and aging: implications for COVID-19 and wound healing[J].Front Immunol,2023,14:1201651.DOI: 10.3389/fimmu.2023.1201651.
    [3] de OliveiraS,RosowskiEE,HuttenlocherA.Neutrophil migration in infection and wound repair: going forward in reverse[J].Nat Rev Immunol,2016,16(6):378-391.DOI: 10.1038/nri.2016.49.
    [4] PhillipsonM,KubesP.The healing power of neutrophils[J].Trends Immunol,2019,40(7):635-647.DOI: 10.1016/j.it.2019.05.001.
    [5] SreejitG,Abdel-LatifA,AthmanathanB,et al.Neutrophil-derived S100A8/A9 amplify granulopoiesis after myocardial infarction[J].Circulation,2020,141(13):1080-1094.DOI: 10.1161/CIRCULATIONAHA.119.043833.
    [6] Ravesloot-ChávezMM,Van DisE,StanleySA.The innate immune response to mycobacterium tuberculosis infection[J].Annu Rev Immunol,2021,39:611-637.DOI: 10.1146/annurev-immunol-093019-010426.
    [7] BorgesL,Pithon-CuriTC,CuriR,et al.COVID-19 and neutrophils: the relationship between hyperinflammation and neutrophil extracellular traps[J].Mediators Inflamm,2020,2020:8829674.DOI: 10.1155/2020/8829674.
    [8] TomlinsonKL,RiquelmeSA,BaskotaSU,et al.Staphylococcus aureus stimulates neutrophil itaconate production that suppresses the oxidative burst[J].Cell Rep,2023,42(2):112064.DOI: 10.1016/j.celrep.2023.112064.
    [9] TumburuL,Ghosh-ChoudharyS,SeifuddinFT,et al.Circulating mitochondrial DNA is a proinflammatory DAMP in sickle cell disease[J].Blood,2021,137(22):3116-3126.DOI: 10.1182/blood.2020009063.
    [10] DenningNL,AzizM,GurienSD,et al.DAMPs and NETs in Sepsis[J].Front Immunol,2019,10:2536.DOI: 10.3389/fimmu.2019.02536.
    [11] MartinKR,WongHL,Witko-SarsatV,et al.G-CSF - A double edge sword in neutrophil mediated immunity[J].Semin Immunol,2021,54:101516.DOI: 10.1016/j.smim.2021.101516.
    [12] LinY,ChenY,FengW,et al.STAT5 promotes chronic pancreatitis by enhancing GM-CSF-dependent neutrophil augmentation[J].J Leukoc Biol,2021,110(2):293-300.DOI: 10.1002/JLB.3MA1020-647R.
    [13] CapucettiA,AlbanoF,BonecchiR.Multiple roles for chemokines in neutrophil biology[J].Front Immunol,2020,11:1259.DOI: 10.3389/fimmu.2020.01259.
    [14] FriedrichM,PohinM,JacksonMA,et al.IL-1-driven stromal-neutrophil interactions define a subset of patients with inflammatory bowel disease that does not respond to therapies[J].Nat Med,2021,27(11):1970-1981.DOI: 10.1038/s41591-021-01520-5.
    [15] LvY,KimK,ShengY,et al.YAP controls endothelial activation and vascular inflammation through TRAF6[J].Circ Res,2018,123(1):43-56.DOI: 10.1161/CIRCRESAHA.118.313143.
    [16] ZhuCL,WangY,LiuQ,et al.Dysregulation of neutrophil death in sepsis[J].Front Immunol,2022,13:963955.DOI: 10.3389/fimmu.2022.963955.
    [17] SurmiakM,Hubalewska-MazgajM,Wawrzycka-AdamczykK,et al.Delayed neutrophil apoptosis in granulomatosis with polyangiitis: dysregulation of neutrophil gene signature and circulating apoptosis-related proteins[J].Scand J Rheumatol,2020,49(1):57-67.DOI: 10.1080/03009742.2019.1634219.
    [18] WestmanJ,GrinsteinS,MarquesPE.Phagocytosis of necrotic debris at sites of injury and inflammation[J].Front Immunol,2019,10:3030.DOI: 10.3389/fimmu.2019.03030.
    [19] 贺伟峰,闫凌峰.巨噬细胞在创面愈合中的调节作用及其相关机制[J].中华烧伤与创面修复杂志,2023,39(2):106-113.DOI: 10.3760/cma.j.cn501225-20230110-00010.
    [20] ChenK,ZhangZ,FangZ,et al.Aged-signal-eliciting nanoparticles stimulated macrophage-mediated programmed removal of inflammatory neutrophils[J].ACS Nano,2023,17(14):13903-13916.DOI: 10.1021/acsnano.3c03815.
    [21] WangJF,WangYP,XieJ,et al.Upregulated PD-L1 delays human neutrophil apoptosis and promotes lung injury in an experimental mouse model of sepsis[J].Blood,2021,138(9):806-810.DOI: 10.1182/blood.2020009417.
    [22] ChenR,ZhouL.PD-1 signaling pathway in sepsis: does it have a future?[J].Clin Immunol,2021,229:108742.DOI: 10.1016/j.clim.2021.108742.
    [23] PanT,SunS,ChenY,et al.Immune effects of PI3K/Akt/HIF-1α-regulated glycolysis in polymorphonuclear neutrophils during sepsis[J].Crit Care,2022,26(1):29.DOI: 10.1186/s13054-022-03893-6.
    [24] OthmanA,SekheriM,FilepJG.Roles of neutrophil granule proteins in orchestrating inflammation and immunity[J].FEBS J,2022,289(14):3932-3953.DOI: 10.1111/febs.15803.
    [25] WillsonJA,ArientiS,SadikuP,et al.Neutrophil HIF-1α stabilization is augmented by mitochondrial ROS produced via the glycerol 3-phosphate shuttle[J].Blood,2022,139(2):281-286.DOI: 10.1182/blood.2021011010.
    [26] PacletMH,LauransS,Dupré-CrochetS.Regulation of neutrophil NADPH oxidase, NOX2: a crucial effector in neutrophil phenotype and function[J].Front Cell Dev Biol,2022,10:945749.DOI: 10.3389/fcell.2022.945749.
    [27] ZengMY,MiraldaI,ArmstrongCL,et al.The roles of NADPH oxidase in modulating neutrophil effector responses[J].Mol Oral Microbiol,2019,34(2):27-38.DOI: 10.1111/omi.12252.
    [28] LiuL,ShaoY,ZhangY,et al.Neutrophil-derived heparin binding protein triggers vascular leakage and synergizes with myeloperoxidase at the early stage of severe burns (With video)[J/OL].Burns Trauma,2021,9:tkab030[2024-03-06].https://pubmed.ncbi.nlm.nih.gov/34646891/.DOI: 10.1093/burnst/tkab030.
    [29] ZhuS,YuY,RenY,et al.The emerging roles of neutrophil extracellular traps in wound healing[J].Cell Death Dis,2021,12(11):984.DOI: 10.1038/s41419-021-04294-3.
    [30] HidalgoA,LibbyP,SoehnleinO,et al.Neutrophil extracellular traps: from physiology to pathology[J].Cardiovasc Res,2022,118(13):2737-2753.DOI: 10.1093/cvr/cvab329.
    [31] OuQ,TanL,ShaoY,et al.Electrostatic charge-mediated apoptotic vesicle biodistribution attenuates sepsis by switching neutrophil NETosis to apoptosis[J].Small,2022,18(20):e2200306.DOI: 10.1002/smll.202200306.
    [32] JinJ,WangF,TianJ,et al.Neutrophil extracellular traps contribute to coagulopathy after traumatic brain injury[J].JCI Insight,2023,8(6):e141110.DOI: 10.1172/jci.insight.141110.
    [33] ShaoY,GuoZ,YangY,et al.Neutrophil extracellular traps contribute to myofibroblast differentiation and scar hyperplasia through the Toll-like receptor 9/nuclear factor Kappa-B/interleukin-6 pathway[J/OL].Burns Trauma,2022,10:tkac044[2024-03-06].https://pubmed.ncbi.nlm.nih.gov/36406661/.DOI: 10.1093/burnst/tkac044.
    [34] DolmaS,KumarH.Neutrophil, extracellular matrix components, and their interlinked action in promoting secondary pathogenesis after spinal cord injury[J].Mol Neurobiol,2021,58(9):4652-4665.DOI: 10.1007/s12035-021-02443-5.
    [35] SolimanAM,BarredaDR.Acute inflammation in tissue healing[J].Int J Mol Sci,2022,24(1):641.DOI: 10.3390/ijms24010641.
    [36] Herrero-CerveraA,SoehnleinO,KenneE.Neutrophils in chronic inflammatory diseases[J].Cell Mol Immunol,2022,19(2):177-191.DOI: 10.1038/s41423-021-00832-3.
    [37] WestbyMJ,DumvilleJC,StubbsN,et al.Protease activity as a prognostic factor for wound healing in venous leg ulcers[J].Cochrane Database Syst Rev,2018,9(9):CD012841.DOI: 10.1002/14651858.CD012841.pub2.
    [38] ZhuY,XiaX,HeQ,et al.Diabetes-associated neutrophil NETosis: pathogenesis and interventional target of diabetic complications[J].Front Endocrinol (Lausanne),2023,14:1202463.DOI: 10.3389/fendo.2023.1202463.
    [39] YangS,WangS,ChenL,et al.Neutrophil extracellular traps delay diabetic wound healing by inducing endothelial-to-mesenchymal transition via the Hippo pathway[J].Int J Biol Sci,2023,19(1):347-361.DOI: 10.7150/ijbs.78046.
    [40] LodgeKM,VassalloA,LiuB,et al.Hypoxia increases the potential for neutrophil-mediated endothelial damage in chronic obstructive pulmonary disease[J].Am J Respir Crit Care Med,2022,205(8):903-916.DOI: 10.1164/rccm.202006-2467OC.
    [41] ChaMJ,HaJ,LeeH,et al.Neutrophil recruitment in arterial thrombus and characteristics of stroke patients with neutrophil-rich thrombus[J].Yonsei Med J,2022,63(11):1016-1026.DOI: 10.3349/ymj.2022.0328.
    [42] DasekeMJ,ChaliseU,Becirovic-AgicM,et al.Neutrophil signaling during myocardial infarction wound repair[J].Cell Signal,2021,77:109816.DOI: 10.1016/j.cellsig.2020.109816.
    [43] HiraoH,NakamuraK,Kupiec-WeglinskiJW.Liver ischaemia-reperfusion injury: a new understanding of the role of innate immunity[J].Nat Rev Gastroenterol Hepatol,2022,19(4):239-256.DOI: 10.1038/s41575-021-00549-8.
    [44] KitchingAR,AndersHJ,BasuN,et al.ANCA-associated vasculitis[J].Nat Rev Dis Primers,2020,6(1):71.DOI: 10.1038/s41572-020-0204-y.
    [45] Shiratori-AsoS,NakazawaD.The involvement of NETs in ANCA-associated vasculitis[J].Front Immunol,2023,14:1261151.DOI: 10.3389/fimmu.2023.1261151.
    [46] AymonnierK,AmslerJ,LamprechtP,et al.The neutrophil: a key resourceful agent in immune-mediated vasculitis[J].Immunol Rev,2023,314(1):326-356.DOI: 10.1111/imr.13170.
    [47] ThitiwuthikiatP,Ta-UeaT,PonghanT,et al.The protective effects of reparixin against endothelial ischemia-reperfusion injury[J].Int J Health Sci (Qassim),2022,16(3):20-24.
    [48] ZarbockA,AllegrettiM,LeyK.Therapeutic inhibition of CXCR2 by Reparixin attenuates acute lung injury in mice[J].Br J Pharmacol,2008,155(3):357-364.DOI: 10.1038/bjp.2008.270.
    [49] HuangY,YangJ,ZhangY,et al.Blocking CXCR1/2 attenuates experimental periodontitis by suppressing neutrophils recruitment[J].Int Immunopharmacol,2024,128:111465.DOI: 10.1016/j.intimp.2023.111465.
    [50] SmolenJS,LandewéR,BergstraSA,et al.EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2022 update[J].Ann Rheum Dis,2023,82(1):3-18.DOI: 10.1136/ard-2022-223356.
    [51] GhigoA,DamilanoF,BracciniL,et al.PI3K inhibition in inflammation: toward tailored therapies for specific diseases[J].Bioessays,2010,32(3):185-196.DOI: 10.1002/bies.200900150.
    [52] NguyenT,DeenickEK,TangyeSG.Phosphatidylinositol 3-kinase signaling and immune regulation: insights into disease pathogenesis and clinical implications[J].Expert Rev Clin Immunol,2021,17(8):905-914.DOI: 10.1080/1744666X.2021.1945443.
    [53] Fresneda AlarconM,McLarenZ,WrightHL.Neutrophils in the pathogenesis of rheumatoid arthritis and systemic Lupus erythematosus: same foe different M.O[J].Front Immunol,2021,12:649693.DOI: 10.3389/fimmu.2021.649693.
    [54] ChmielinskaJJ,KramerJH,MakIT,et al.Substance P receptor blocker, aprepitant, inhibited cutaneous and other neurogenic inflammation side effects of the EGFR1-TKI, erlotinib[J].Mol Cell Biochem,2020,465(1/2):175-185.DOI: 10.1007/s11010-019-03677-7.
    [55] KimDJ,MoonJY,KimSM,et al.Substance P improves renal ischemia reperfusion injury through modulating immune response[J].Front Immunol,2020,11:600.DOI: 10.3389/fimmu.2020.00600.
    [56] MohammadA,BabikerF,Al-BaderM.Effects of Apocynin, a NADPH oxidase inhibitor, in the protection of the heart from ischemia/reperfusion injury[J].Pharmaceuticals (Basel),2023,16(4):492.DOI: 10.3390/ph16040492.
    [57] DenormeF,PortierI,RustadJL,et al.Neutrophil extracellular traps regulate ischemic stroke brain injury[J].J Clin Invest,2022,132(10):e154225.DOI: 10.1172/JCI154225.
    [58] LiuX,ArfmanT,WichapongK,et al.PAD4 takes charge during neutrophil activation: impact of PAD4 mediated NET formation on immune-mediated disease[J].J Thromb Haemost,2021,19(7):1607-1617.DOI: 10.1111/jth.15313.
    [59] SilvaC,WanderleyC,VerasFP,et al.Gasdermin D inhibition prevents multiple organ dysfunction during sepsis by blocking NET formation[J].Blood,2021,138(25):2702-2713.DOI: 10.1182/blood.2021011525.
    [60] BalićA,VlašićD,ŽužulK,et al.Omega-3 versus omega-6 polyunsaturated fatty acids in the prevention and treatment of inflammatory skin diseases[J].Int J Mol Sci,2020,21(3):741.DOI: 10.3390/ijms21030741.
    [61] LiC,WuX,LiuS,et al.Role of resolvins in the inflammatory resolution of neurological diseases[J].Front Pharmacol,2020,11:612.DOI: 10.3389/fphar.2020.00612.
    [62] ShinoharaM,KibiM,RileyIR,et al.Cell-cell interactions and bronchoconstrictor eicosanoid reduction with inhaled carbon monoxide and resolvin D1[J].Am J Physiol Lung Cell Mol Physiol,2014,307(10):L746-757.DOI: 10.1152/ajplung.00166.2014.
    [63] MatteA,RecchiutiA,FedertiE,et al.Resolution of sickle cell disease-associated inflammation and tissue damage with 17R-resolvin D1[J].Blood,2019,133(3):252-265.DOI: 10.1182/blood-2018-07-865378.
  • 加载中
图(1)
计量
  • 文章访问数:  6
  • HTML全文浏览量:  3
  • PDF下载量:  1
  • 被引次数: 0
出版历程
  • 收稿日期:  2024-03-06
  • 网络出版日期:  2024-04-26

目录

    /

    返回文章
    返回