高迁移率族蛋白B1与变应性鼻炎的相关性

doi:10.6040/j.issn.1673-3770.0.2020.031

摘要/Abstract

摘要： 变应性鼻炎(AR)是IgE介导的鼻黏膜的非感染性炎性疾病,其特征是炎症介质的上调和鼻黏膜的炎症细胞浸润。HMGB1作为典型的警报蛋白和损伤相关模式分子,在介导炎症反应、细胞迁移、组织侵袭等中起着多种作用。目前关于HMGB1与变应性疾病的研究主要集中在系统性红斑狼疮、哮喘、特应性皮炎中,对于其在AR中的作用尚有争议,论文就近年来有关学者对HMGB1在AR发病机制中的相关研究进行总结。

关键词: 高迁移率族蛋白B1, 变应性鼻炎, 发病机制, 炎症, 受体, 信号通路

Abstract: Allergic rhinitis(AR)is a noninfectious inflammatory disease of the nasal mucosa mediated by IgE and characterized by the upregulation of inflammatory mediators and infiltration of inflammatory cells in the nasal mucosa. As a typical warning protein and damage-related model molecule, high-mobility group box-1(HMGB1)plays a variety of roles in mediating inflammatory response, cell migration, and tissue invasion. Currently, studies on HMGB1 and allergic diseases mainly focus on systemic lupus erythematosus, asthma, and atopic dermatitis, whereas the role of HMGB1 in AR is still controversial. This article summarizes the relevant researches on the role of HMGB1 in the pathogenesis of AR.

Key words: High mobility group box-1, Allergic rhinitis, Pathogenesis, Inflammation, Receptor, Signal pathway

中图分类号:

R765.21

朱正茹,张小兵. 高迁移率族蛋白B1与变应性鼻炎的相关性[J]. 山东大学耳鼻喉眼学报, 2020, 34(6): 123-128.

ZHU Zhengru,ZHANG Xiaobing. Correlation between high-mobility group box-1 and allergic rhinitis[J]. Journal of Otolaryngology and Ophthalmology of Shandong University, 2020, 34(6): 123-128.

参考文献

[1] 程雷, 钱俊俊, 田慧琴. 变应性鼻炎研究的若干进展[J]. 山东大学耳鼻喉眼学报, 2017, 31(3): 1-3. doi:10.6040/j.issn.1673-3770.1.2017.021. CHENG Lei, QIAN Junjun, TIAN Huiqin. Research progresses on allergic rhinitis[J]. Journal of Otolaryngology and Ophthalmology of Shandong University, 2017, 31(3): 1-3. doi:10.6040/j.issn.1673-3770.1.2017.021.
[2] Andersson U, Yang H, Harris H. Extracellular HMGB1 as a therapeutic target in inflammatory diseases[J]. Expert Opin Ther Targets, 2018, 22(3): 263-277. doi:10.1080/14728222.2018.1439924.
[3] Fritz G. RAGE: a single receptor fits multiple ligands[J]. Trends Biochem Sci, 2011, 36(12): 625-632. doi:10.1016/j.tibs.2011.08.008.
[4] Ullah MA, Loh Z, Gan WJ, et al. Receptor for advanced glycation end products and its ligand high-mobility group box-1 mediate allergic airway sensitization and airway inflammation[J]. J Allergy Clin Immunol, 2014, 134(2): 440-450. doi:10.1016/j.jaci.2013.12.1035.
[5] Huang WF, Zhao HJ, Dong HM, et al. High-mobility group box 1 impairs airway epithelial barrier function through the activation of the RAGE/ERK pathway[J]. Int J Mol Med, 2016, 37(5): 1189-1198. doi:10.3892/ijmm.2016.2537.
[6] Zhu XW, Cong JN, Yang B, et al. Association analysis of high-mobility group box-1 protein 1(HMGB1)/toll-like receptor(TLR)4 with nasal interleukins in allergic rhinitis patients[J]. Cytokine, 2020, 126: 154880. doi:10.1016/j.cyto.2019.154880.
[7] Yuan Y, Liu Q, Zhao J, et al. SIRT1 attenuates murine allergic rhinitis by downregulated HMGB 1/TLR4 pathway[J]. Scand J Immunol, 2018, 87(6): e12667. doi:10.1111/sji.12667.
[8] Tang HP, Li TT, Han XL, et al. TLR4 antagonist ameliorates combined allergic rhinitis and asthma syndrome(CARAS)by reducing inflammatory monocytes infiltration in mice model[J]. Int Immunopharmacol, 2019, 73: 254-260. doi:10.1016/j.intimp.2019.05.021.
[9] Shimizu S, Kouzaki H, Kato T, et al. HMGB1-TLR4 signaling contributes to the secretion of interleukin 6 and interleukin 8 by nasal epithelial cells[J]. Am J Rhinol Allergy, 2016, 30(3): 167-172. doi:10.2500/ajra.2016.30.4300.
[10] Jiang Huanhuan, Duan Junyan, Xu Kaihong, et al. Resveratrol protects against asthma-induced airway inflammation and remodeling by inhibiting the HMGB1/TLR4/NF-κB pathway[J]. Experimental and therapeutic medicine vol, 2019,18(1): 459-466. doi: 10.3892/etm.2019.7594.
[11] Zhang Han, Yang Nan, Wang Tianyue, et al. Vitamin D reduces inflammatory response in asthmatic mice through HMGB1/TLR4/NFκB signaling pathway[J].Molecular Medicine Reportsvol, 2018, 17(2): 2915-2920. doi: 10.3892/mmr.2017.8216.
[12] 陈删. 高迁移率家族蛋白1在小鼠过敏性鼻炎及急性细菌性鼻窦炎中的表达及其意义[D]. 武汉: 华中科技大学, 2016. CHEN Shan. The role of high mobility group box 1 protein in murine allergic rhinitis and acute bacterial rhinosinusitis[D]. Wuhan: Huazhong University of Science and Technology, 2016.
[13] Liang Y, Hou CC, Kong JL, et al. HMGB1 binding to receptor for advanced glycation end products enhances inflammatory responses of human bronchial epithelial cells by activating p38 MAPK and ERK1/2[J]. Mol Cell Biochem, 2015, 405(1/2): 63-71. doi:10.1007/s11010-015-2396-0.
[14] 徐韶飞, 聂晚频, 姚凯, 等. HMGB1促进血管平滑肌细胞增殖与迁移的机制研究[J]. 中国普通外科杂志, 2015, 24(12): 1703-1708. doi: 10.3978/j.issn.1005-6947.2015.12.013. XU Shaofei, NIE Wanpin, YAO Kai, et al. Mechanism for HMGB1 in promoting migration and proliferation of vascular smooth muscle cells[J]. Chinese Journal of General Surgery, 2015, 24(12): 1703-1708. doi: 10.3978/j.issn.1005-6947.2015.12.013.
[15] 吴欣阳, 朱宏岩, 吴革平. PI3K/PKB通道在肥大细胞介导的过敏性鼻炎中的多重作用[J]. 临床医药文献电子杂志, 2017, 4(72): 14255-14256. doi:10.16281/j.cnki.jocml.2017.72.163.
[16] Zhang YL, You B, Liu XZ, et al. High-mobility group box 1(HMGB1)induces migration of endothelial progenitor cell via receptor for advanced glycation end-products(RAGE)-dependent PI3K/akt/Enos signaling pathway[J]. Med Sci Monit, 2019, 25: 6462-6473. doi:10.12659/MSM.915829.
[17] Lee CC, Lai YT, Chang HT, et al. Inhibition of high-mobility group box 1 in lung reduced airway inflammation and remodeling in a mouse model of chronic asthma[J]. Biochem Pharmacol, 2013, 86(7): 940-949. doi:10.1016/j.bcp.2013.08.003.
[18] Chen YC, Statt S, Wu RE, et al. High mobility group box 1-induced epithelial mesenchymal transition in human airway epithelial cells[J]. Sci Rep, 2016, 6: 18815. doi:10.1038/srep18815.
[19] Kim TH, Lee JY, Lee HM, et al. Remodelling of nasal mucosa in mild and severe persistent allergic rhinitis with special reference to the distribution of collagen, proteoglycans, and lymphatic Vessels[J]. Clin Exp Allergy, 2010, 40(12): 1742-54. doi: 10.1111/j.1365-2222.2010.03612.x.
[20] Cavone L, Cuppari C, Manti S, et al. Increase in the level of proinflammatory cytokine HMGB1 in nasal fluids of patients with rhinitis and its sequestration by glycyrrhizin induces eosinophil cell death[J]. Clin Exp Otorhinolaryngol, 2015, 8(2): 123-128. doi:10.3342/ceo.2015.8.2.123.
[21] 刘阳, 王志斌, 刘争, 等. 高迁移率族蛋白B1在变应性鼻炎中的表达及意义[J]. 中国免疫学杂志, 2010, 26(7): 651-654. LIU Yang, WANG Zhibin, LIU Zheng, et al. doi: CNKI:SUN:ZMXZ.0.2010-07-018. The expression of HMGB1 in nasal mucosa of allergic rhinitis patients and its significance[J]. Chinese Journal of Immunology, 2010, 26(7): 651-654. doi: CNKI:SUN:ZMXZ.0.2010-07-018.
[22] Lu B, Wang C, Wang M, et al. Molecular mechanism and therapeutic modulation of high mobility group box 1 release and action: an updated review[J]. Expert Rev Clin Immunol, 2014, 10(6): 713-727. doi:10.1586/1744666X.2014.909730.
[23] Pellegrini L, Xue JM, Larson D, et al. HMGB1 targeting by ethyl pyruvate suppresses malignant phenotype of human mesothelioma[J]. Oncotarget, 2017, 8(14): 22649-22661. doi:10.18632/oncotarget.15152.
[24] Seo MS, Kim HJ, Kim H, et al. Ethyl pyruvate directly attenuates active secretion of HMGB1 in proximal tubular cells via induction of heme oxygenase-1[J]. J Clin Med, 2019, 8(5): E629. doi:10.3390/jcm8050629.
[25] Liu YY, Chen NH, Chang CH, et al. Ethyl pyruvate attenuates ventilation-induced diaphragm dysfunction through high-mobility group box-1 in a murine endotoxaemia model[J]. J Cell Mol Med, 2019, 23(8): 5679-5691. doi:10.1111/jcmm.14478.
[26] Wagner N, Dieteren S, Franz N, et al. Ethyl pyruvate ameliorates hepatic injury following blunt chest trauma and hemorrhagic shock by reducing local inflammation, NF-kappaB activation and HMGB1 release[J]. PLoS One, 2018, 13(2): e0192171. doi:10.1371/journal.pone.0192171.
[27] Chen S, Wang YJ, Gong GQ, et al. Ethyl pyruvate attenuates murine allergic rhinitis partly by decreasing high mobility group box 1 release[J]. Exp Biol Med(Maywood), 2015, 240(11): 1490-1499. doi:10.1177/1535370214566563.
[28] Bhat SM, Massey N, Karriker LA, et al. Ethyl pyruvate reduces organic dust-induced airway inflammation by targeting HMGB1-RAGE signaling[J]. Respir Res, 2019, 20(1): 27. doi:10.1186/s12931-019-0992-3.
[29] Shin JH, Kim ID, Kim SW, et al. Ethyl pyruvate inhibits HMGB1 phosphorylation and release by chelating calcium[J]. Mol Med, 2015, 20: 649-657. doi:10.2119/molmed.2014.00039.
[30] Chen D, Bellussi LM, Cocca S, et al. Glycyrrhetinic acid suppressed hmgb1 release by up-regulation of Sirt6 in nasal inflammation[J]. J Biol Regul Homeost Agents, 2017, 31(2): 269-277.
[31] Bellussi LM, Cocca S, Passali GC, et al. HMGB1 in the pathogenesis of nasal inflammatory diseases and its inhibition as new therapeutic approach: a review from the literature[J]. Int Arch Otorhinolaryngol, 2017, 21(4): 390-398. doi:10.1055/s-0036-1597665.

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