切换至 "中华医学电子期刊资源库"

中华实验和临床感染病杂志(电子版) ›› 2018, Vol. 12 ›› Issue (05) : 417 -421. doi: 10.3877/cma.j.issn.1674-1358.2018.05.001

所属专题: 文献

综述

Siglecs家族在脓毒症中的研究进展
褚萨萨1, 尤娜2, 汪茂荣1,()   
  1. 1. 210000 南京市,南京中医药大学附属八一医院感染科
    2. 236800 亳州市,亳州市人民医院感染科
  • 收稿日期:2018-01-30 出版日期:2018-10-15
  • 通信作者: 汪茂荣
  • 基金资助:
    军队特需药品保密专项"十二五"计划(No. 2013ZX09J13110-05B)

Progress on Siglecs in sepsis

Sasa Chu1, Na You2, Maorong Wang1,()   

  1. 1. Infection Department, University of Ttraditional Chinese Affiliated to 81 Hospital, Nanjing 210000, China
    2. Infection Department, Bozhou People’s Hospital, Bozhou 236800, China
  • Received:2018-01-30 Published:2018-10-15
  • Corresponding author: Maorong Wang
  • About author:
    Corresponding author: Wang Maorong, Email:
引用本文:

褚萨萨, 尤娜, 汪茂荣. Siglecs家族在脓毒症中的研究进展[J/OL]. 中华实验和临床感染病杂志(电子版), 2018, 12(05): 417-421.

Sasa Chu, Na You, Maorong Wang. Progress on Siglecs in sepsis[J/OL]. Chinese Journal of Experimental and Clinical Infectious Diseases(Electronic Edition), 2018, 12(05): 417-421.

Siglecs家族是表达于免疫细胞表面的跨膜受体,在感染性疾病中发挥调节免疫平衡的作用。脓毒症是炎症诱导的器官功能障碍,其发病机理包括免疫调节紊乱、炎症反应以及凝血功能障碍等。本文主要就Siglecs家族在脓毒症发病机理中的作用进行综述。Siglec-1、Siglec-5和Siglec-14通过启动炎症反应和免疫反应发挥双向效应。Siglec-2通过调节B细胞和T细胞在脓毒症中调节免疫平衡。Siglec-9通过Toll样受体4(TLR4)的内吞作用调节巨噬细胞的极化现象,进而抑制中性粒细胞的作用。Siglec-10抑制危险相关分子模式(DAMP),帮助T细胞启动抗原抗体反应,减少B细胞数量从而减弱炎症反应。Siglecs在脓毒症不同阶段的功能具有潜在治疗意义。

Siglecs are cell surface transmenbrane receptor and are expressed on the immune cells, which regulated the immune balance in inflammation diseases. Sepsis is organ dysfunction induced by infection, the pathogenesis of sepsis contains the immune disorder, inflammatory reaction and coagulation dysregulation. In this article, we reviewed the role of Siglecs in the pathogenesis of sepsis was reviewed. Siglec-1, Siglec-5 and Siglec-14 play bidirectional role by regulating the inflammation and immunity. Siglec-2 modulates the immune balance in inflammation through regulating B cell and T cell response. Siglec-9 modulates macrophagepolarization and restrain the function of neutrophils during infection through the endocytosis of toll-like receptor 4 (TLR4). Siglec-10 inhibits the danger-associated molecular pattern (DAMP) and helps T cells initiate antigen-antibody responses, and reduces the number of B cells, thus reducing inflammation. Modulation of Siglecs function in different stages of sepsis have potential therapeutic significance in the treatment of sepsis.

[10]
Wu Y, Lan C, Ren D, et al. Induction of siglec-1 by endotoxin tolerance suppresses the innate immune response by promoting TGF-β1 production[J]. J Biol Chem,2016,291(23):12370-12382.
[11]
Sewald X, Ladinsky MS, Uchil PD, et al. Retroviruses use CD169-mediated trans-infection of permissive lymphocytes to establish infection[J]. Science,2015,350(6260):563-567.
[12]
Walker JA, Smith KG. CD22: an inhibitory enigma[J]. Immunology, 2008,123(3):314-325.
[13]
Gjertsson I, Nitschke L, Tarkowski A. The role of B cell CD22 expression in Staphylococcus aureus arthritis and sepsis[J]. Microbes Infect,2004,6(4):377-382.
[14]
Jiang YN, Cai X, Zhou HM, et al. Diagnostic and prognostic roles of soluble CD22 in patients with Gram-negative bacterial sepsis[J]. Hepatobiliary Pancreat Dis Int,2015,14(5):523-529.
[15]
Jiang Y, Zhou H, Ma D, et al. MicroRNA-19a and CD22 comprise a feedback loop for B cell response in sepsis[J]. Med Sci Monit,2015,21:1548-1555.
[16]
Ma DY, Suthar MS, Kasahara S, et al. CD22 is required for protection against West Nile virus Infection[J]. J Virol,2013,87(6):3361-3375.
[17]
Nitschke L. Suppressing the antibody response with Siglec ligands[J]. N Engl J Med,2013,369(14):1373-1374.
[18]
Kreitman RJ, Squires DR, Stetler-Stevenson M, et al. PhaseⅠtrial of recombinant immunotoxin RFB4 (dsFv)-PE38 (BL22) in patients with B-cell malignancies[J]. J Clin Oncol,2005,23(27):6719-6729.
[19]
Shao JY, Yin WW, Zhang QF, et al. Siglec-7 defines a highly functional natural killer cell subset and inhibits cell-mediated activities[J]. Scand J Immunol,2016,84(3):182-190.
[20]
Mizrahi S, Gibbs BF, Karra L, et al. Siglec-7 is an inhibitory receptor on human mast cells and basophils[J]. J Allergy Clin Immunol,2014,134(1):230-233.
[21]
Nguyen KA, Hamzeh-Cognasse H, Palle S, et al. Role of Siglec-7 in apoptosis in human platelets[J]. PLoS One,2014,9(9):e106239.
[22]
Grutkoski PS, Chen Y, Chung CS, et al. Sepsis-induced SOCS-3 expression is immunologically restricted to phagocytes[J]. J Leukoc Biol,2003,74(5):916-922.
[23]
Orr SJ, Morgan NM, Buick RJ, et al. SOCS3 targets Siglec 7 for proteasomal degradation and blocks Siglec 7-mediated responses[J]. J Biol Chem,2007,282(6):3418-3422.
[24]
Varchetta S, Brunetta E, Roberto A, et al. Engagement of Siglec-7 receptor induces a pro-inflammatory response selectively in monocytes[J]. PLoS One,2012,7(9):e45821.
[25]
Siddiqui S, Schwarz F, Springer S, et al. Studies on the detection, expression, glycosylation, dimerization, and ligand binding properties of mouse Siglec-E[J]. J Biol Chem,2017,292(3):1029-1037.
[26]
Liu YC, Zou XB, Chai YF, et al. Macrophage polarization in inflammatory diseases[J]. Int J Biol Sci,2014,10(5):520-529.
[27]
Liu YC, Yao FH, Chai YF, et al. Xuebijing injection promotes M2 polarization of macrophages and improves survival rate in septic mice[J]. Evid Based Complement Alternat Med,2015,2015:352642.
[28]
Higuchi H, Shoji T, Murase Y, et al. Siglec-9 modulated IL-4 responses in the macrophage cell line RAW264[J]. Biosci Biotechnol Biochem,2016,80(3):501-509.
[29]
Higuchi H, Shoji T, Iijima S, et al. Constitutively expressed Siglec-9 inhibits LPS-induced CCR7, but enhances IL-4-induced CD200R expression in human macrophages[J]. Biosci Biotechnol Biochem,2016,80(6):1141-1148.
[30]
Chen GY, Brown NK, Wu W, et al. Broad and direct interaction between TLR and Siglec families of pattern recognition receptors and its regulation by Neu1[J]. Elife,2014,3:e04066.
[31]
Boyd CR, Orr SJ, Spence S, et al. Siglec-E is up-regulated and phosphorylated following lipopolysaccharide stimulation in order to limit TLR-driven cytokine production[J]. J Immunol, 2009,183(12):7703-7709.
[32]
Wu Y, Ren D, Chen GY. Siglec-E negatively regulates the activation of TLR4 by controlling its endocytosis[J]. J Immunol,2016,197(8): 3336-3347.
[33]
McMillan SJ, Sharma RS, Richards HE, et al. Siglec-E promotesβ2-integrin-dependent NADPH oxidase activation to suppress neutrophil recruitment to the lung[J]. J Biol Chem,2014,289(29):20370-20376.
[34]
Aalto K, Autio A, Kiss EA, et al. Siglec-9 is a novel leukocyte ligand for vascular adhesion protein-1 and can be used in PET imaging of inflammation and cancer[J]. Blood,2011,118(13):3725-3733.
[35]
Spence S, Greene MK, Fay F, et al. Targeting Siglecs with a sialic acid-decorated nanoparticle abrogates inflammation[J]. Sci Transl Med,2015,7(303):303ra140.
[36]
Chu S, Zhu X, You N, et al. The Fab fragment of a human anti-Siglec-9 monoclonal antibody suppresses LPS-induced inflammatory responses in human macrophages[J]. Front Immunol,2016,7:649-661.
[37]
Chen GY, Brown NK, Zheng P, et al. Siglec-G/10 in self-nonself discrimination of innate and adaptive immunity[J]. Glycobiology, 2014,24(9):800-806.
[38]
Stephenson HN, Mills DC, Jones H, et al. Pseudaminic acid onCampylobacter jejuniflagella modulates dendritic cell IL-10 expression via Siglec-10 receptor: a novel flagellin-host interaction[J]. J Infect Dis,2014,210(9):1487-1498.
[39]
Chen W, Han C, Xie B, et al. Induction of Siglec-G by RNA viruses inhibits the innate immune response by promoting RIG-I degradation[J]. Cell,2013,152(3):467-478.
[1]
Schauer R. Sialic acids as regulators of molecular and cellular interactions[J]. Curr Opin Struct Biol,2009,19(5):507-514.
[2]
Macauley MS, Crocker PR, Paulson JC.Siglec-mediated regulation of immune cell function in disease[J]. Nat Rev Immunol,2014,14(10):653-666.
[3]
Cao H, de Bono B, Belov K, et al. Comparative genomics indicates the mammalian CD33rSiglec locus evolved by an ancient large-scale inverse duplication and suggests all Siglecs share a common ancestral region[J]. Immunogenetics,2009,61(5):401-417.
[40]
Parlato M, Souza-Fonseca-Guimaraes F, Philippart F, et al. CD24-triggered caspase-dependent apoptosis via mitochondrial membrane depolarization and reactive oxygen species production of human neutrophils is impaired in sepsis[J]. J Immunol,2014,192(5):2449-2459.
[41]
Chen GY, Tang J, Zheng P, et al. CD24 and Siglec-10 selectively repress tissue damage-induced immune responses[J].Science, 2009,323(5922):1722-1725.
[42]
Chen GY, Chen X, King S, et al. Amelioration of sepsis by inhibiting sialidase-mediated disruption of the CD24-Siglec-G interaction[J]. Nat Biotechnol,2011,29(5):428-435.
[43]
Paulson JC, Kawasaki N. Sialidase inhibitors DAMPen sepsis[J]. Nat Biotechnol,2011,29(5):406-407.
[44]
Ding Y, Guo Z, Liu Y, et al. The lectin Siglec-G inhibits dendritic cell cross-presentation by impairing MHC classⅠ-peptide complex formation[J]. Nat Immunol,2016,17(10):1167-1175.
[45]
Bandala-Sanchez E, Zhang Y, Reinwald S, et al. T cell regulation mediated by interaction of soluble CD52 with the inhibitory receptor Siglec-10[J]. Nat Immunol,2013,14(7):741-748.
[46]
Nitschke L. Siglec-G is a B-1 cell inhibitory receptor and also controls B cell tolerance[J]. Ann N Y Acad Sci,2015,1362:117-121.
[47]
Jellusova J, Düber S, Gückel E, et al. Siglec-G regulates B1 cell survival and selection[J]. J Immunol,2010,185(6):3277-3284.
[48]
Carlin AF, Chang YC, Areschoug T, et al. Group BStreptococcus suppression of phagocyte functions by protein-mediated engagement of human Siglec-5[J]. J Exp Med,2009,206(8):1691-1699.
[49]
Ali SR, Fong JJ, Carlin AF, et al. Siglec-5 and Siglec-14 are polymorphic paired receptors that modulate neutrophil and amnion signaling responses to group BStreptococcus[J]. J Exp Med,2014,211(6):1231-1242.
[50]
Angata T, Ishii T, Motegi T, et al. Loss of Siglec-14 reduces the risk of chronic obstructive pulmonary disease exacerbation[J]. Cell Mol Life Sci,2013,70(17):3199-3210.
[51]
Wielgat P, Mroz RM, Stasiak-Barmuta A, et al. Inhaled corticosteroids increase siglec-5/14 expression in sputum cells of COPD patients[J].Adv Exp Med Biol,2015,839:1-5.
[4]
Rhodes A, Evans LE, Alhazzani W, et al. Surviving sepsis campaign: international guidelines for management of sepsis and septic shock: 2016[J]. Crit Care Med,2017,45(3):486-552.
[5]
Boomer JS, To K, Chang KC, et al. Immunosuppression in patients who die of sepsis and multiple organ failure[J]. JAMA,2011,306(23):2594-2605.
[6]
Izquierdo-Useros N, Lorizate M, Contreras FX, et al. Sialyllactose in viral membrane gangliosides is a novel molecular recognition pattern for mature dendritic cell capture of HIV-1[J]. PLoS Biol,2012,10(4):e1001315.
[7]
Gummuluru S, Pina RNG, Akiyama H. CD169-dependent cell-associated HIV-1 transmission: a driver of virus dissemination[J]. J Infect Dis,2014,210 (Suppl 3):S641-S647.
[8]
Gupta P, Lai SM, Sheng J, et al. Tissue-resident CD169(+) macrophages form a crucial front line against plasmodium Infection[J]. Cell Rep,2016,16(6):1749-1761.
[9]
Shaabani N, Duhan V, Khairnar V, et al. CD169+macrophages regulate PD-L1 expression via type I interferon and thereby prevent severe immunopathology after LCMV infection[J]. Cell Death Dis,2016,7(11):e2446.
[1] 农云洁, 黄小桂, 黄裕兰, 农恒荣. 超声在多重肺部感染诊断中的临床应用价值[J/OL]. 中华医学超声杂志(电子版), 2024, 21(09): 872-876.
[2] 王振宇, 张洪美, 荆琳, 何名江, 闫奇. 膝骨关节炎相关炎症因子与血浆代谢物间的因果关系及中介效应[J/OL]. 中华损伤与修复杂志(电子版), 2024, 19(06): 467-473.
[3] 张洁, 罗小霞, 余鸿. 系统性免疫炎症指数对急性胰腺炎患者并发器官功能损伤的预测价值[J/OL]. 中华普外科手术学杂志(电子版), 2025, 19(01): 68-71.
[4] 唐梅, 周丽, 牛岑月, 周小童, 王倩. ICG荧光导航的腹腔镜肝切除术临床意义[J/OL]. 中华普外科手术学杂志(电子版), 2024, 18(06): 655-658.
[5] 许月芳, 刘旺, 曾妙甜, 郭宇姝. 多粘菌素B和多粘菌素E治疗外科多重耐药菌感染临床疗效及安全性分析[J/OL]. 中华普外科手术学杂志(电子版), 2024, 18(06): 700-703.
[6] 付成旺, 杨大刚, 王榕, 李福堂. 营养与炎症指标在可切除胰腺癌中的研究进展[J/OL]. 中华普外科手术学杂志(电子版), 2024, 18(06): 704-708.
[7] 梁孟杰, 朱欢欢, 王行舟, 江航, 艾世超, 孙锋, 宋鹏, 王萌, 刘颂, 夏雪峰, 杜峻峰, 傅双, 陆晓峰, 沈晓菲, 管文贤. 联合免疫治疗的胃癌转化治疗患者预后及术后并发症分析[J/OL]. 中华普外科手术学杂志(电子版), 2024, 18(06): 619-623.
[8] 皮尔地瓦斯·麦麦提玉素甫, 李慧灵, 艾克拜尔·艾力, 李赞林, 王志, 克力木·阿不都热依木. 生物补片修补巨大复发性腹壁切口疝临床疗效分析[J/OL]. 中华疝和腹壁外科杂志(电子版), 2024, 18(06): 624-628.
[9] 顾熙, 徐子宇, 周澍, 张吴楼, 张业鹏, 林昊, 刘宗航, 嵇振岭, 郑立锋. 腹股沟疝腹膜前间隙无张力修补术后补片感染10 例报道[J/OL]. 中华疝和腹壁外科杂志(电子版), 2024, 18(06): 665-669.
[10] 高娟, 徐建庆, 闫芳, 丁盛华, 刘霞. Rutkow、TAPP、TEP 手术治疗单侧腹股沟疝患者的临床疗效及对血清炎症因子水平的影响[J/OL]. 中华疝和腹壁外科杂志(电子版), 2024, 18(06): 675-680.
[11] 孙璐, 蒋亚玲, 陈凌君. 布托啡诺对脑缺血再灌注损伤大鼠神经炎症和JAK2/STAT3信号通路的影响[J/OL]. 中华细胞与干细胞杂志(电子版), 2024, 14(06): 344-350.
[12] 中华医学会器官移植学分会. 肝移植术后缺血性胆道病变诊断与治疗中国实践指南[J/OL]. 中华肝脏外科手术学电子杂志, 2024, 13(06): 739-748.
[13] 王湛, 李文坤, 杨奕, 徐芳, 周敏思, 苏珈仪, 王亚丹, 吴静. 炎症指标在早发性结直肠肿瘤中的应用[J/OL]. 中华临床医师杂志(电子版), 2024, 18(09): 802-810.
[14] 贾玲玲, 滕飞, 常键, 黄福, 刘剑萍. 心肺康复在各种疾病中应用的研究进展[J/OL]. 中华临床医师杂志(电子版), 2024, 18(09): 859-862.
[15] 颜世锐, 熊辉. 感染性心内膜炎合并急性肾损伤患者的危险因素探索及死亡风险预测[J/OL]. 中华临床医师杂志(电子版), 2024, 18(07): 618-624.
阅读次数
全文


摘要