POS0136 ROLES OF AUTOPHAGY IN THE PATHOGENESIS OF PRIMARY GOUTY ARTHRITIS

Background: Gout is a chronic autoinflammatory disease caused by monosodium urate (MSU) crystal deposition [1].Acute gout characterized an acute inflammatory reaction that resolves spontaneously within few days[2], which one of the distinguishing features compared to other arthropathies or self-inflammatory diseases. Autophagy lysosomal degradation pathway essential for cellular growth, survival, differentiation, development and homeostasis [3]. Studies have demonstrated autophagy might play key role in pathogenesis primary gouty arthritis (GA) [4-7]. However, roles not yet been elucidated. Objectives: The aim our study was investigate changes autophagy-related gene (ATG) mRNA protein patients clinical importance these genes explore GA. Methods: expression levels ATGs (ATG3, ATG7, ATG10, ATG5, ATG12, ATG16L1, ATG4B LC3-2) were measured peripheral blood mononuclear cells (PBMCs) from 196 subjects, including 57 (AG group), intercritical (IG group) 82 healthy control subjects (HC group). relationship between ATG laboratory analyzed GA patients. Results: ATG4B, ATG10 LC3-2 much lower AG group than IG HC groups (p<0.05), while ATG7 level higher (p<0.05). LC3-2, ATG3, groups, those ATG16L1 far In patients, correlated with metabolic indexes. Conclusion: Altered suggests involved participates regulating inflammation metabolism. References: [1]Dalbeth N, Choi HK, Joosten LAB, Khanna PP, Matsuo H, Perez-Ruiz F, et al. Gout. Nat Rev Dis Primers. 2019;5: 69.doi:10.1038/s41572-019-0115-y. [2]Schauer C, Janko Munoz LE, Zhao Y, Kienhöfer D, Frey B, Aggregated neutrophil extracellular traps limit degrading cytokines chemokines. Med. 2014;20: 511-517.doi:10.1038/nm.3547. [3]Han Zhang L, Xing Chen X, Tang P, relieves function inhibition apoptosis-promoting effects on osteoblast induced glucocorticoid. Int J Mol 2018;41: 800-808. doi:10.3892/ijmm.2017.3270. [4]Yang QB, He YL, Zhong XW, Xie WG, Zhou JG. Resveratrol ameliorates via upregulation sirtuin 1 promote Inflammopharmacology. 2019;27: 47-56.doi:10.1007/s10787-018-00555-4. [5]Mitroulis I, Kambas K, Chrysanthopoulou A, Skendros Apostolidou E, Kourtzelis Neutrophil trap formation associated IL-1β signaling gout. PLoS One. 2011;6: e29318.doi: 10.1371/journal.pone.0029318. [6]Crişan TO, Cleophas MCP, Novakovic Erler van de Veerdonk FL, Stunnenberg HG, Uric acid priming human monocytes driven AKT-PRAS40 pathway. Proc Natl Acad Sci U S A. 2017;114: 5485-5490.doi:10.1073/pnas.1620910114. [7]Lee SS, Lee SW, Oh DH, Kim HS, Chae SC, SK. Genetic analysis rs2241880(T > C) polymorphism susceptibility Clin Rheumatol. 2019;25: e113-e115.doi:10.1097/rhu.0000000000000685. Disclosure Interests: Yu-Qin Huang: None declared, Quan-Bo Grant/research support from: National Natural Science Foundation China(General Program) (no.81974250) Technology Plan Project Sichuan Province (no.2018JY0257), Jian-Xiong Zheng: gui-lin jian: tao-hong liu: Xin He: fan-ni xiao: qin xiong: Yu-Feng Qing Nanchong City (no.18SXHZ0522)