白介素-33在急性呼吸窘迫综合征中的研究进展被引量：6

Research progress of interleukin-33 in acute respiratory distress syndrome

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摘要急性呼吸窘迫综合征（acute respiratory distress syndrome,ARDS）是以顽固性低氧血症和进行性呼吸困难为主要临床特点的综合征,是危重症患者死亡的主要原因之一。尽管,近年来医疗技术的迅猛发展和新的药物的应用使ARDS的预后有所改善,但其病死率仍高达40%~50%。因此,更充分的了解ARDS的发病机制,实现早期诊断,为临床上ARDS的防治提供指导仍是呼吸和重症医学界研究的重点和热点。白介素（interleukin,IL）-33是新近发现的IL-1家族成员,在炎症、感染、自身免疫性疾病等多种疾病中发挥重要的警报素作用,促进机体的炎症反应,加重机体组织的损伤。故IL-33及其信号通路可能成为阻断炎症通路的级联反应的一个潜在的分子靶点。本文就IL-33在ARDS中的研究进展做一综述。 Acute respiratory distress syndrome（ARDS）is a clinical syndrome characterized by refractory hypoxemia and progressive dyspnea. It is one of the leading causes of death in critically illed patients. In recent years,although the rapid development of medical technology and the application of new drugs have improved the prognosis of ARDS,the mortality of ARDS is still as high as 40%-50%. Therefore,it is still the focus and hotpot in the research of respiratory and intensive medicine to further understand the pathogenesis of ARDS,achieve early diagnosis,and provide guidance for the prevention and treatment of ARDS. Interleukin-33（IL-33）is a recently discovered member of the Interleukin-1（IL-1）family. It plays a crucial role as an alarmins in inflammation,infection,au toimmune disease and many other diseases,enlarges the body＇s inflammatory response,and aggravate tissue injury. Therefore,IL-33 and its signal pathway probably become potential molecular targets to block the cascade of inflammatory pathways in the treatment of ARDS. In this paper,we reviewed on the role of IL-33 in ARDS.

作者付娟徐昉

机构地区重庆医科大学附属第一医院急诊医学科和重症医学科

出处《重庆医科大学学报》 CAS CSCD 北大核心 2016年第4期425-428,共4页 Journal of Chongqing Medical University

基金国家自然科学基金资助项目(编号:81570069)

关键词急性呼吸窘迫综合症白介素-33 细胞因子警报素信号通路 acute respiratory distress syndrome interleukin-33 cytokines alarmins signal pathway

分类号 R563.8 [医药卫生—呼吸系统]

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1Liew FY,Pitman NI, McInnes IB. Disease-associated functions of IL-33 :the new kid in the IL-1 family[J]. Nat Rev Immunol,2010,10 (2) : 103-110.
2Moussion C,Ortega N,Girard JP. The IL-1-like cytokine IL-33 is constitutively expressed in the nucleus of endothelial cells and epithelial cells in vivo:a novel ‘alarmin'?[J]. PLoS One,2008,3(10):e3331.
3Haraldsen G, Balogh J,Pollheimer J, et al. Interleukin-33-cytokine of dual function or novel alarmin?[J]. Trends Immunol,2009,30(5): 227-233.
4Carriere V,Roussel L,Ortega N,et al. IL-33,the IL-1-like cy- tokine ligand for ST2 receptor,is a chromatin-associated nuclear factor in vivo[J]. Proc Natl Acad Sci U S A,2007,104(1) :282-287.
5Villar J,Sulemanji D,Kacmarek RM. The acute respiratory distress syndrome:incidence and mortality,has it changed?[J]. Curr Opin Crit Cave,2014,20(1) :3-9.
6Comet AD, Hofstra JJ, Vlaar AP, et al. Activated protein C attenu- ates pulmonary coagulopathy in patients with acute respiratory distress syndrome[J]. J Thromb Haemost, 2013,11 (5) : 894-901.
7Kajstura J,Rota M,Hall SR,et al. Evidence for human lung stem cells[J]. N Engl J Med, 2011, 364(19) : 1795-1806.
8Bao Z,Ye Q,Gong W,et al. Humanized monoclonal antibody against the chemokine CXCL-8(IL-8) effectively prevents acute lung injury[J]. Int Immunopharmacol, 2010,10 (2) : 259-263.
9Taniguchi K,Yamamoto S,Hitomi E,et al. Interleukin 33 is induced by tumor necrosis factor alpha and interferon gamma in keratinocytes and contributes to allergic contact dermatitis[J]. J Investig Allergol ClinImmunol,2013,23(6) :428-434.
10Kuchler AM,Pollheimer J,Balogh J,et al. Nuclear interleukin- 33 is generally expressed in resting endothelium but rapidly lost upon angiogenie or proinflammatory activation[J]. Am J Pathol, 2008,173 (4): 1229-1242.