中性粒细胞生理与病理生理作用再认识

孙炳伟; 黄佳敏

doi:10.3760/cma.j.cn501120-20211122-00391

中性粒细胞生理与病理生理作用再认识

doi: 10.3760/cma.j.cn501120-20211122-00391

孙炳伟^,,
黄佳敏

南京医科大学附属苏州医院烧伤整形科，苏州　　215002

基金项目:

国家自然科学基金重大项目 U21A20370

国家自然科学基金面上项目 82072217, 81772135

江苏省基础研究计划（自然科学基金）专项 BK20201178

详细信息

通讯作者:
孙炳伟，Email：sunbinwe@hotmail.com

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- 被引次数: 0
出版历程
- 收稿日期: 2021-11-22

Re-understanding the physiological and pathophysiological roles of neutrophils

Sun Bingwei^,,
Huang Jiamin

Department of Burns and Plastic Surgery, Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou 215002, China

Funds:

Major Program of National Natural Science Foundation of China U21A20370

General Program of National Natural Science Foundation of China 82072217, 81772135

Special Program of Basic Research Plan (Natural Science Foundation) of Jiangsu Province of China BK20201178

More Information

Corresponding author: Sun Bingwei, Email: sunbinwe@hotmail.com

摘要

摘要: 中性粒细胞一直被认为是先天免疫系统中一种短寿命的、同质的细胞类型，具有有限的促/抗炎作用。然而最近10年，随着研究的深入，对中性粒细胞的了解正在经历着某种复兴。对中性粒细胞的异质性及其与其他免疫细胞相互作用机制的研究促进了研究者对中性粒细胞生理与病理生理作用的再认识。在接下来的数十年中，随着单细胞测序技术、空间转录组测序技术以及多组学联合测序技术的发展，研究者将对中性粒细胞的生物学行为认识得更为透彻。本文对近年来中性粒细胞的多种生物学行为及其在多种疾病中的作用进行简要评述。
- 细胞死亡 /
- 趋化作用 /
- 异质性 /
- 中性粒细胞
Abstract: Neutrophils have always been considered as a short-lived and homogeneous cell type in the innate immune system, which have limited pro-inflammatory or anti-inflammatory effects. However, in recent 10 years, the understanding of neutrophils has been undergoing some kind of revival as researches progressed. The researches on the heterogeneity of neutrophils and the mechanism of their interaction with other immune cells have promoted the researchers to re-understand the physiological and pathophysiological roles of neutrophils. In the following decades, with the development of single-cell sequencing technology, spatial transcriptome sequencing technology, and multi-omics combined sequencing technology, researchers will have a better understanding of the biological behaviors of neutrophils. This paper briefly reviews the biological behaviors of neutrophils and their roles in various diseases in recent years.
- Cell death /
- Chemotaxis /
- Hetero- geneity /
- Neutrophils
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参考文献(47)

[1]	AmulicB, CazaletC, HayesGL, et al. Neutrophil function: from mechanisms to disease[J]. Annu Rev Immunol, 2012,30:459-489. DOI: 10.1146/annurev-immunol-020711-074942.
[2]	PetriB, SanzMJ. Neutrophil chemotaxis[J]. Cell Tissue Res, 2018,371(3):425-436. DOI: 10.1007/s00441-017-2776-8.
[3]	FoxS, LeitchAE, DuffinR, et al. Neutrophil apoptosis: relevance to the innate immune response and inflammatory disease[J]. J Innate Immun, 2010,2(3):216-227. DOI: 10.1159/000284367.
[4]	RobertsRE, HallettMB. Neutrophil cell shape change: mechanism and signalling during cell spreading and phagocytosis[J]. Int J Mol Sci, 2019,20(6):1383.DOI: 10.3390/ijms20061383.
[5]	MollinedoF. Neutrophil degranulation, plasticity, and cancer metastasis[J]. Trends Immunol, 2019,40(3):228-242. DOI: 10.1016/j.it.2019.01.006.
[6]	RosalesC. Neutrophils at the crossroads of innate and adaptive immunity[J]. J Leukoc Biol, 2020,108(1):377-396. DOI: 10.1002/JLB.4MIR0220-574RR.
[7]	KolaczkowskaE, KubesP. Neutrophil recruitment and function in health and inflammation[J]. Nat Rev Immunol, 2013,13(3):159-175. DOI: 10.1038/nri3399.
[8]	NavegantesKC, de Souza GomesR, PereiraPAT, et al. Immune modulation of some autoimmune diseases: the critical role of macrophages and neutrophils in the innate and adaptive immunity[J]. J Transl Med, 2017,15(1):36. DOI: 10.1186/s12967-017-1141-8.
[9]	RosalesC. Neutrophil: a cell with many roles in inflammation or several cell types?[J]. Front Physiol, 2018,9:113. DOI: 10.3389/fphys.2018.00113.
[10]	LiewPX, KubesP. The neutrophil's role during health and disease[J]. Physiol Rev, 2019,99(2):1223-1248. DOI: 10.1152/physrev.00012.2018.
[11]	GalliSJ, BorregaardN, WynnTA. Phenotypic and functional plasticity of cells of innate immunity: macrophages, mast cells and neutrophils[J]. Nat Immunol, 2011,12(11):1035-1044. DOI: 10.1038/ni.2109.
[12]	Silvestre-RoigC, FridlenderZG, GlogauerM, et al. Neutrophil diversity in health and disease[J]. Trends Immunol, 2019,40(7):565-583. DOI: 10.1016/j.it.2019.04.012.
[13]	HellebrekersP, VrisekoopN, KoendermanL. Neutrophil phenotypes in health and disease[J]. Eur J Clin Invest, 2018,48 Suppl 2(Suppl Suppl 2):e12943. DOI: 10.1111/eci.12943.
[14]	XieX, ShiQ, WuP, et al. Single-cell transcriptome profiling reveals neutrophil heterogeneity in homeostasis and infection[J]. Nat Immunol, 2020,21(9):1119-1133. DOI: 10.1038/s41590-020-0736-z.
[15]	QiX, YuY, SunR, et al. Identification and characterization of neutrophil heterogeneity in sepsis[J]. Crit Care, 2021,25(1):50. DOI: 10.1186/s13054-021-03481-0.
[16]	GieseMA, HindLE, HuttenlocherA. Neutrophil plasticity in the tumor microenvironment[J]. Blood, 2019,133(20):2159-2167. DOI: 10.1182/blood-2018-11-844548.
[17]	CarvalhoLO, AquinoEN, NevesAC, et al. The neutrophil nucleus and its role in neutrophilic function[J]. J Cell Biochem, 2015,116(9):1831-1836. DOI: 10.1002/jcb.25124.
[18]	MortazE, AlipoorSD, AdcockIM, et al. Update on neutrophil function in severe inflammation[J]. Front Immunol, 2018,9:2171. DOI: 10.3389/fimmu.2018.02171.
[19]	De FilippoK, RankinSM. CXCR4, the master regulator of neutrophil trafficking in homeostasis and disease[J]. Eur J Clin Invest, 2018,48 Suppl 2(Suppl Suppl 2):e12949. DOI: 10.1111/eci.12949.
[20]	UderhardtS, MartinsAJ, TsangJS, et al. Resident macrophages cloak tissue microlesions to prevent neutrophil-driven inflammatory damage[J]. Cell, 2019,177(3):541-555.e17. DOI: 10.1016/j.cell.2019.02.028.
[21]	SaffarzadehM, JuenemannC, QueisserMA, et al. Neutrophil extracellular traps directly induce epithelial and endothelial cell death: a predominant role of histones[J]. PLoS One, 2012,7(2):e32366. DOI: 10.1371/journal.pone.0032366.
[22]	WangX, QinW, XuX, et al. Endotoxin-induced autocrine ATP signaling inhibits neutrophil chemotaxis through enhancing myosin light chain phosphorylation[J]. Proc Natl Acad Sci U S A, 2017,114(17):4483-4488. DOI: 10.1073/pnas.1616752114.
[23]	YangY, LiuL, GuoZ, et al. A novel computer vision-based assessment of neutrophil chemotaxis in patients with severe infection[J]. Clin Transl Immunology, 2021,10(8):e1333. DOI: 10.1002/cti2.1333.
[24]	SpaanAN, SurewaardBG, NijlandR, et al. Neutrophils versus Staphylococcus aureus: a biological tug of war[J]. Annu Rev Microbiol, 2013,67:629-650. DOI: 10.1146/annurev-micro-092412-155746.
[25]	NowickaD, GrywalskaE. Staphylococcus aureus and host immunity in recurrent furunculosis[J]. Dermatology, 2019,235(4):295-305. DOI: 10.1159/000499184.
[26]	CurleyG, ContrerasMM, NicholAD, et al. Hypercapnia and acidosis in sepsis: a double-edged sword?[J]. Anesthesiology, 2010,112(2):462-472. DOI: 10.1097/ALN.0b013e3181ca361f.
[27]	MetzemaekersM, GouwyM, ProostP. Neutrophil chemoattractant receptors in health and disease: double-edged swords[J]. Cell Mol Immunol, 2020,17(5):433-450. DOI: 10.1038/s41423-020-0412-0.
[28]	LarsonRC, MausMV. Recent advances and discoveries in the mechanisms and functions of CAR T cells[J]. Nat Rev Cancer, 2021,21(3):145-161. DOI: 10.1038/s41568-020-00323-z.
[29]	MittalM, SiddiquiMR, TranK, et al. Reactive oxygen species in inflammation and tissue injury[J]. Antioxid Redox Signal, 2014,20(7):1126-1167. DOI: 10.1089/ars.2012.5149.
[30]	BenjaminJT, PlosaEJ, SucreJM, et al. Neutrophilic inflammation during lung development disrupts elastin assembly and predisposes adult mice to COPD[J]. J Clin Invest, 2021,131(1):e139481.DOI: 10.1172/JCI139481.
[31]	CuiC, ChakrabortyK, TangXA, et al. Neutrophil elastase selectively kills cancer cells and attenuates tumorigenesis[J]. Cell, 2021,184(12):3163-3177.e21. DOI: 10.1016/j.cell.2021.04.016.
[32]	HuhSJ, LiangS, SharmaA, et al. Transiently entrapped circulating tumor cells interact with neutrophils to facilitate lung metastasis development[J]. Cancer Res, 2010,70(14):6071-6082. DOI: 10.1158/0008-5472.CAN-09-4442.
[33]	TazzymanS, NiazH, MurdochC. Neutrophil-mediated tumour angiogenesis: subversion of immune responses to promote tumour growth[J]. Semin Cancer Biol, 2013,23(3):149-158. DOI: 10.1016/j.semcancer.2013.02.003.
[34]	GranotZ, HenkeE, ComenEA, et al. Tumor entrained neutrophils inhibit seeding in the premetastatic lung[J]. Cancer Cell, 2011,20(3):300-314. DOI: 10.1016/j.ccr.2011.08.012.
[35]	López-LagoMA, PosnerS, ThodimaVJ, et al. Neutrophil chemokines secreted by tumor cells mount a lung antimetastatic response during renal cell carcinoma progression[J]. Oncogene, 2013,32(14):1752-1760. DOI: 10.1038/onc.2012.201.
[36]	NjeimR, AzarWS, FaresAH, et al. NETosis contributes to the pathogenesis of diabetes and its complications[J]. J Mol Endocrinol, 2020,65(4):R65-R76. DOI: 10.1530/JME-20-0128.
[37]	WongSL, DemersM, MartinodK, et al. Diabetes primes neutrophils to undergo NETosis, which impairs wound healing[J]. Nat Med, 2015,21(7):815-819. DOI: 10.1038/nm.3887.
[38]	ScappaticcioL, MaiorinoMI, MaioA, et al. Neutropenia in patients with hyperthyroidism: systematic review and meta-analysis[J]. Clin Endocrinol (Oxf), 2021,94(3):473-483. DOI: 10.1111/cen.14313.
[39]	DrewW, WilsonDV, SapeyE. Inflammation and neutrophil immunosenescence in health and disease: targeted treatments to improve clinical outcomes in the elderly[J]. Exp Gerontol, 2018,105:70-77. DOI: 10.1016/j.exger.2017.12.020.
[40]	邱雨璐, 刘牧, 王灵冰, 等. 中性粒细胞免疫衰老与老年病的相关性研究进展[J].中国老年学杂志,2019,39(8):2019-2023.DOI: 10.3969/j.issn.1005-9202.2019.08.072.
[41]	SapeyE, GreenwoodH, WaltonG, et al. Phosphoinositide 3-kinase inhibition restores neutrophil accuracy in the elderly: toward targeted treatments for immunosenescence[J]. Blood, 2014,123(2):239-248. DOI: 10.1182/blood-2013-08-519520.
[42]	SapeyE, PatelJM, GreenwoodHL, et al. Pulmonary infections in the elderly lead to impaired neutrophil targeting, which is improved by simvastatin[J]. Am J Respir Crit Care Med, 2017,196(10):1325-1336. DOI: 10.1164/rccm.201704-0814OC.
[43]	PatelJM, ThickettDR, GaoF, et al. Statins for sepsis: distinguishing signal from the noise when designing clinical trials[J]. Am J Respir Crit Care Med, 2013,188(7):874. DOI: 10.1164/rccm.201302-0392LE.
[44]	WangJ. Neutrophils in tissue injury and repair[J]. Cell Tissue Res, 2018,371(3):531-539. DOI: 10.1007/s00441-017-2785-7.
[45]	JunJI, KimKH, LauLF. The matricellular protein CCN1 mediates neutrophil efferocytosis in cutaneous wound healing[J]. Nat Commun, 2015,6:7386. DOI: 10.1038/ncomms8386.
[46]	BrubakerAL, RendonJL, RamirezL, et al. Reduced neutrophil chemotaxis and infiltration contributes to delayed resolution of cutaneous wound infection with advanced age[J]. J Immunol, 2013,190(4):1746-1757. DOI: 10.4049/jimmunol.1201213.
[47]	NguyenKT, SethAK, HongSJ, et al. Deficient cytokine expression and neutrophil oxidative burst contribute to impaired cutaneous wound healing in diabetic, biofilm-containing chronic wounds[J]. Wound Repair Regen, 2013,21(6):833-841. DOI: 10.1111/wrr.12109.