中性粒细胞胞外诱捕网在系统性红斑狼疮相关间质性肺病中的作用
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作者单位:

(1. 武汉大学人民医院胸外科,武汉430060;2. 武汉大学第一临床学院,武汉430060)


Role of neutrophil extracellular traps in systemic lupus erythematosus-associated interstitial lung disease
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Affiliation:

(1. Department of Thoracic Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, China;2. First Clinical College of Wuhan University, Wuhan 430060, China)

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    【摘要】中性粒细胞参与病原体清除与早期炎症反应,是免疫系统的重要组成部分。但近年来越来越多的研究表明,中性粒细胞通过形成中性粒细胞胞外诱捕网(NETs)介导炎症反应并促进纤维化的形成,在自身免疫性疾病和间质性肺病(ILD)的发病机制中的作用逐渐受到重视。本文首先介绍NETs的结构、功能和形成过程,并结合NETs在其他自身免疫病中的作用,总结NETs参与系统性红斑狼疮(SLE)相关ILD针对NETs的发病机制,最后提出了自身免疫性疾病相关ILD针对NETs的潜在治疗靶点。

    基金项目:国家自然科学基金面上项目(82170106);中国器官移植发展基金(2020HX0011);中央高校基本科研业务费专项资金(2042021kf1038)

    【Abstract】Neutrophils, involved in pathogen clearance and early inflammatory responses, are an important part of the immune system. However, in recent years, more and more studies have shown that neutrophils mediate inflammatory responses and promote fibrosis by forming neutrophil extracellular traps (NETs), and their role in the pathogenesis of autoimmune diseases and pulmonary interstitial fibrosis has been attracting attention. The review first introduces the structures, functions, and formation of NETs, then summarizes their role in systemic lupus erythematosus-associated interstitial lung disease (SLE-ILD) in reference to the pathogenesis of other autoimmune diseases, and finally proposes prospective therapeutic targets of NETs in autoimmune disease-related ILD.

    This work was supported by the General Project of National Natural Science Foundation of China (82170106), China Organ Transplantation Development Foundation (2020HX0011) and the Fundamental Research Funds for the Central Universities(2042021kf1038).

    参考文献
    [1] Mittoo S, Fell CD.Pulmonary manifestations of systemic lupus erythematosus[J].Semin Respir Crit Care Med, 2014,35(2):249-254.DOI:10.1055/s-0034-1371537.
    [2] Lopez Velazquez M, Highland KB.Pulmonary manifestations of systemic lupus erythematosus and Sjgren′s syndrome[J].Curr Opin Rheumatol, 2018,30(5):449-464.DOI:10.1097/BOR.0000000000000531.
    [3] Hannah JR, D′Cruz DP.Pulmonary complications of systemic lupus erythematosus[J].Semin Respir Crit Care Med, 2019,40(2):227-234.DOI:10.1055/s-0039-1685537.
    [4] Nielepkowicz-Go'zdzińska A, Fendler W, Robak E, et al.The role of CXC chemokines in pulmonary fibrosis of systemic lupus erythematosus patients[J].Arch Immunol Ther Exp (Warsz), 2015,63(6):465-473.DOI:10.1007/s00005-015-0356-8.
    [5] Fujimori Y, Kataoka M, Tada S, et al.The role of interleukin-8 in interstitial pneumonia[J].Respirology, 2003,8(1):33-40.DOI:10.1046/j.1440-1843.2003.00420.x.
    [6] Brinkmann V, Reichard U, Goosmann C, et al.Neutrophil extracellular traps kill bacteria[J].Science, 2004,303(5663):1532-1535.DOI:10.1126/science.1092385.
    [7] Chrysanthopoulou A, Mitroulis I, Apostolidou E, et al.Neutrophil extracellular traps promote differentiation and function of fibroblasts[J].J Pathol, 2014,233(3):294-307.DOI:10.1002/path.4359.
    [8] Frangou E, Chrysanthopoulou A, Mitsios A, et al.REDD1/autophagy pathway promotes thromboinflammation and fibrosis in human systemic lupus erythematosus (SLE) through NETs decorated with tissue factor (TF) and interleukin-17A (IL-17A)[J].Ann Rheum Dis, 2019,78(2):238-248.DOI:10.1136/annrheumdis-2018-213181.
    [9] Mutua V,Gershwin LJ.A review of neutrophil extracellular traps (NETs) in disease:potential anti-NETs therapeutics[J].Clin Rev Allergy Immunol, 2021,61(2):194-211.DOI:10.1007/s12016-020-08804-7.
    [10] Thiam HR, Wong SL, Wagner DD, et al.Cellular mechanisms of NETosis[J].Annu Rev Cell Dev Biol, 2020,36:191-218.DOI:10.1146/annurev-cellbio-020520-111016.
    [11] Jorch SK, Kubes P.An emerging role for neutrophil extracellular traps in noninfectious disease[J].Nat Med, 2017,23(3):279-287.DOI:10.1038/nm.4294.
    [12] Lood C, Blanco LP, Purmalek MM, et al.Neutrophil extracellular traps enriched in oxidized mitochondrial DNA are interferogenic and contribute to lupus-like disease[J].Nat Med, 2016,22(2):146-153.DOI:10.1038/nm.4027.
    [13] Delgado-Rizo V, Martínez-Guzmán MA, Iiguez-Gutierrez L, et al.Neutrophil extracellular traps and its implications in infla-mmation:an overview[J].Front Immunol, 2017,8:81.DOI:10.3389/fimmu.2017.00081.
    [14] Yousefi S, Mihalache C, Kozlowski E, et al.Viable neutrophils release mitochondrial DNA to form neutrophil extracellular traps[J].Cell Death Differ, 2009,16(11):1438-1444.DOI:10.1038/cdd.2009.96.
    [15] McIlroy DJ, Jarnicki AG, Au GG, et al.Mitochondrial DNA neutrophil extracellular traps are formed after trauma and subsequent surgery[J].J Crit Care, 2014,29(6):1133.e1-e5.DOI:10.1016/j.jcrc.2014.07.013.
    [16] Liu L, Mao Y, Xu B, et al.Induction of neutrophil extracellular traps during tissue injury:involvement of STING and Toll-like receptor 9 pathways[J].Cell prolif, 2019,52(3):e12579.DOI:10.1111/cpr.12579.
    [17] Mallavia B, Liu F, Lefranais E, et al.Mitochondrial DNA stimulates TLR9-dependent neutrophil extracellular trap formation in primary graft dysfunction[J].Am J Respir Cell Mol Biol, 2020,62(3):364-372.DOI:10.1165/rcmb.2019-0140OC.
    [18] Bengtsson AA, Pettersson, Wichert S, et al.Low production of reactive oxygen species in granulocytes is associated with organ damage in systemic lupus erythematosus[J].Arthritis Res Ther, 2014,16(3):R120.DOI:10.1186/ar4575.
    [19] Wirestam L, Arve S, Linge P, et al.Neutrophils-important communicators in systemic lupus erythematosus and antiphospholipid syndrome[J].Front Immunol, 2019,10:2734.DOI:10.3389/fimmu.2019.02734.
    [20] Villanueva E, Yalavarthi S, Berthier CC, et al.Netting neutrophils induce endothelial damage, infiltrate tissues, and expose immunostimulatory molecules in systemic lupus erythematosus[J].J Immunol, 2011,187(1):538-552.DOI:10.4049/jimmunol.1100450.
    [21] Kaplan MJ.Neutrophils in the pathogenesis and manifestations of SLE[J].Nat Rev Rheumatol, 2011,7(12):691-699.DOI:10.1038/nrrheum.2011.132.
    [22] Mistry P, Nakabo S, O′Neil L, et al.Transcriptomic, epigenetic, and functional analyses implicate neutrophil diversity in the pathogenesis of systemic lupus erythematosus[J].Proc Natl Acad Sci USA, 2019,116(50):25222-25228.DOI:10.1073/pnas.1908576116.
    [23] Hakkim A, Fürnrohr BG, Amann K, et al.Impairment of neutrophil extracellular trap degradation is associated with lupus nephritis[J].Proc Natl Acad Sci USA, 2010,107(21):9813-9818.DOI:10.1073/pnas.0909927107.
    [24] Suzuki M, Ikari J, Anazawa R, et al.PAD4 deficiency improves bleomycin-induced neutrophil extracellular traps and fibrosis in mouse lung[J].Am J Respir Cell Mol Biol, 2020,63(6):806-818.DOI:10.1165/rcmb.2019-0433OC.
    [25] Spagnolo P, Distler O, Ryerson CJ, et al.Mechanisms of progressive fibrosis in connective tissue disease (CTD)-associated interstitial lung diseases (ILDs)[J].Ann Rheum Dis, 2021,80(2):143-150.DOI:10.1136/annrheumdis-2020-217230.
    [26] Meng XM, Nikolic-Paterson DJ, Lan HY.TGF-β:the master regulator of fibrosis[J].Nat Rev Nephrol, 2016,12(6):325-338.DOI:10.1038/nrneph.2016.48.
    [27] Lyv Q, Wang J, Xu C, et al.Pirfenidone alleviates pulmonary fibrosis in vitro and in vivo through regulating Wnt/GSK-3β/β-catenin and TGF-β1/Smad2/3 signaling pathways[J].Mol Med, 2020,26(1):49.DOI:10.1186/s10020-020-00173-3.
    [28] An ZJ, Li JW, Yu JB, et al.Neutrophil extracellular traps induced by IL-8 aggravate atherosclerosis via activation of NF-κB signaling in macrophages[J].Cell Cycle, 2019,18(21):2928-2938.DOI:10.1080/15384101.2019.1662678.
    [29] Ye Q, Chen B, Tong Z, et al.Thalidomide reduces IL-18, IL-8 and TNF-alpha release from alveolar macrophages in interstitial lung disease[J].Eur Respir J, 2006,28(4):824-831.DOI:10.1183/09031936.06.00131505.
    [30] Wang H, Zhang Y, Wang Q, et al.The regulatory mechanism of neutrophil extracellular traps in cancer biological behavior[J].Cell Biosci, 2021,11(1):193.DOI:10.1186/s13578-021-00708-z.
    [31] Zhang S, Shu X, Tian X, et al.Enhanced formation and impaired degradation of neutrophil extracellular traps in dermatomyositis and polymyositis:a potential contributor to interstitial lung disease complications[J].Clin Exp Immunol, 2014,177(1):134-141.DOI:10.1111/cei.12319.
    [32] Zhang S, Jia X, Zhang Q, et al.Neutrophil extracellular traps activate lung fibroblast to induce polymyositis-related interstitial lung diseases via TLR9-miR-7-Smad2 pathway[J].J Cell Mol Med, 2020,24(2):1658-1669.DOI:10.1111/jcmm.14858.
    [33] Gazdhar A, Lebrecht D, Roth M, et al.Time-dependent and somatically acquired mitochondrial DNA mutagenesis and respiratory chain dysfunction in a scleroderma model of lung fibrosis[J].Sci Rep, 2014,4:5336.DOI:10.1038/srep05336.
    [34] Jaeger VK, Lebrecht D, Nicholson AG, et al.Mitochondrial DNA mutations and respiratory chain dysfunction in idiopathic and connective tissue disease-related lung fibrosis[J].Sci Rep, 2019,9(1):5500.DOI:10.1038/s41598-019-41933-4.
    [35] Porto BN, Stein RT.Neutrophil extracellular traps in pulmonary diseases:too much of a good thing?[J].Front Immunol, 2016,7:311.DOI:10.3389/fimmu.2016.00311.
    [36] Knight JS, Subramanian V, O′Dell AA, et al.Peptidylarginine deiminase inhibition disrupts NET formation and protects against kidney, skin and vascular disease in lupus-prone MRL/lpr mice[J].Ann Rheum Dis, 2015,74(12):2199-2206.DOI:10.1136/annrheumdis-2014-205365.
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孙宇石,杨森,林慧庆.中性粒细胞胞外诱捕网在系统性红斑狼疮相关间质性肺病中的作用[J].中华老年多器官疾病杂志,2022,21(9):699-703

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  • 收稿日期:2021-10-10
  • 在线发布日期: 2022-09-30
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