2021 07 v.56 1167-1171
痛风性关节炎发病的炎性机制研究进展
基金项目(Foundation):
国家自然科学基金(编号：81671601、81771774)
邮箱(Email):
lixiangpei55@126.com;
DOI:
10.19405/j.cnki.issn1000-1492.2021.07.032
中文作者单位:
安徽医科大学附属省立医院风湿免疫科;
摘要(Abstract):
该文综述了导致痛风性关节炎发病的多种炎症细胞与细胞因子之间的关联、toll样受体介导的信号通路、ATP-P2X7R通路、NALP3炎性小体等在急性痛风性关节炎发病过程中的重要作用,急性炎症缓解的分子机制及秋水仙碱抑制炎症信号通路的新机制,为未来治疗急性痛风性关节炎提供了新依据。
关键词(KeyWords):
痛风;MSU;IL-1β;炎症细胞;NALP3炎性小体;ATP-P2X7R通路
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参考文献
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[2]Han H,Qiao Q,Dong Y,et al.The prevalence of hyperuricemia in a population of the coastal city of Qingdao,China[J].J Rheumatol,2006,33(7):1346-50．
[3]Tao J H,Zhang Y,Li X P.P2XYR:a potential key regulator of acute gouty arthritis[J].Semin Arthritis Rheum,2013,43(3):376-80．
[4]Hall C J,Sanderson L E,Lawrence L M,et al.Blocking fatty acid-fueled mROS production within macrophages alleviates acute gouty inflammation[J].J Clin Invest,2018,128 (5):1752-71．
[5]Joosten L A,Netea M G,Mylona,et al.Engagement of fatty acids with Toll-like receptor 2 drives interleukin-1βproduction via the ASC/caspase 1 pathway in monosodium urate monohydrate crystalinduced gouty arthritis[J].Arthritis Rheum,2010,62 (11):3237-48．
[6]Liu Y,Zhao Q,Yin Y,et al.Serum levels of IL-17 are elevated in patients with acute gouty arthritis[J].Biochem Biophys Res Commun,2018,497(3):897-902．
[7]Mills K H,Dungan L S,Jones S A,et al.The role of inflammasome-derived IL-1 in driving IL-17 responses[J].J Leukoc Biol,2013,93(4):489-97．
[8]Rudensky A Y.Regulatory T cells and Foxp3[J].Immunol Rev,2011,241(1):260-8．
[9]Dai X J,Tao J H,Li X P,et al.Changes of Treg/Th17 ratio in spleen of acute gouty arthritis[J].Inflammation,2018,41 (5):1955-64．
[10]Joosten L A,Abdollahi-Roodsaz S,Dinarello C A,et al.Toll-like receptors and chronic inflammation in rheumatic diseases:new developments[J].Nat Rev Rheumatol,2016,12(6):344-57．
[11]Mylona E E,Mouktaroudi M,Crisan T O,et al.Enhanced interleukin-1βproduction of PBMCs from patients with gout after stimulation with toll-like receptor-2 ligands and urate crystals[J].Arthritis Res Ther,2012,14(4):R158．
[12]Hecker A,Küllmar M,Wilker S,et al.Phosphocholine-modified macromolecules and canonical nicotinic agonists inhibit ATP-induced IL-1βrelease[J].J Immunol,2015,195(5):2325-34．
[13]Ainscough J S,Gerberick G F,Kimber I,et al.Interleukin-1βprocessing is dependent on a calcium-mediated interaction with calmodulin[J].J Biol Chem,2015,290(52):31151-61．
[14]Dostert C,Pétrilli V,Van Bruggen R,et al.Innate immune activation through nalp3 inflammasome sensing of asbestos and silica[J].Science,2008,320(5876):674-7．
[15]Bae J Y,Park H H.Crystal structure of NALP3 protein pyrin domain (PYD) and its implications in inflammasome assembly[J].J Biol Chem,2011,286(45):39528-36．
[16]Hornung V,Bauernfeind F,Halle A,et al.Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization[J].Nat Immunol,2008,9(8):847-56．
[17]Shi C S,Shenderov K,Huang N N,et al.Activation of autophagy by inflammatory signals limits IL-1βproduction by targeting ubiquitinated inflammasomes for destruction[J].Nat Immunol,2012,13(3):255-63．
[18]Marchetti C,Swartzwelter B,Koenders M I,et al.NLRP3 inflammasome inhibitor OLT1177 suppresses joint inflammation in murine models of acute arthritis[J].Arthritis Res Ther,2018,20(1):169．
[19]Nomura J,So A,Tamura M,et al.Intracellular ATP decrease mediates NLRP3 inflammasome activation upon nigericin and crystal stimulation[J].J Immunol,2015,195(12):5718-24．
[20]Steiger S,Harper J L.Mechanisms of spontaneous resolution of acute gouty inflammation[J].Curr Rheumatol Rep,2014,16 (1):392．
[21]Zhao T Y,Lv X X,Cao L,et al.Renal excretion is a cause of decreased serum uric acid during acute gout[J].Int J Rheum Dis,2018,21(9):1723-27．
[22]Rose D M,Sydlaske A D,Agha-Babakhani A,et al.Transglutaminase 2 limits murine peritoneal acute gout-like inflammation by regulating macrophage clearance of apoptotic neutrophils[J].Arthritis Rheum,2006,54(10),3363-71．
[23]Rada B.Neutrophil Extracellular Traps and Microcrystals[J].JImmunol Res,2017,2017:1-7．
[24]Zeng M,Dang W,Zhao M,et al.IL-37 inhibits the production of pro-inflammatory cytokines in MSU crystal-induced inflammatory response[J].Clin Rheumatol,2016,35(9):2251-8．
[25]Cavalli G,Dinarello C A.Suppression of inflammation and acquired immunity by IL-37[J].Immunol Rev,2018,281(1):179-90．
[26]Marques-da-Silva C,Chaves M M,Castro N G,et al.Colchicine inhibits cationic dye uptake induced by ATP in P2X2 and P2X7receptor-expressing cells:implications for its therapeutic action[J].Br J Pharmacol,2011,163(5):912-26．
[27]Slobodnick A,Shah B,Pillinger M H,et al.Colchicine:old and new[J].Am J Med,2015,128(5):461-70.
基本信息:
DOI：10.19405/j.cnki.issn1000-1492.2021.07.032
中图分类号:R589.7
引用信息:
[1]潘显阳,陶金辉,李向培.痛风性关节炎发病的炎性机制研究进展[J].安徽医科大学学报,2021,56(07):1167-1171.DOI:10.19405/j.cnki.issn1000-1492.2021.07.032.
基金信息:
国家自然科学基金(编号：81671601、81771774)