山东大学耳鼻喉眼学报 ›› 2022, Vol. 36 ›› Issue (3): 123-129.doi: 10.6040/j.issn.1673-3770.0.2021.463

• 研究进展 • 上一篇    下一篇

细胞焦亡在变应性鼻炎中的作用机制及研究进展

刘真1,2,宋西成1,2   

  1. 1. 青岛大学附属烟台毓璜顶医院 耳鼻咽喉头颈外科, 山东 烟台 264000;
    2. 山东省耳鼻喉疾病临床医学研究中心, 山东 烟台 264000
  • 发布日期:2022-06-15
  • 通讯作者: 宋西成. E-mail:songxicheng@126.com
  • 基金资助:
    国家自然科学基金面上项目(82071021);山东省重点研发计划(重大科技创新工程)项目(2020CXGC011302)

Mechanisms and research progress of pyroptosis in allergic rhinitis

LIU Zhen1,2Overview,SONG Xicheng1,2   

  1. 1. Department of Otorhinolaryngology & Head and Neck Surgery, Yantai Yuhuangding Hospital, Qingdao University, Yantai 264000, Shandong, China;
    2. Shandong Provincial Clinical Research Center for Otorhinolaryngologic Diseases, Yantai 264000, Shandong, China
  • Published:2022-06-15

摘要: 变应性鼻炎(AR)是由环境和遗传因素共同作用导致的鼻黏膜变应性炎症疾病,目前AR的发病率呈现每年不断升高的趋势,给人们的身心健康、生活等造成严重的影响,其主要的治疗手段包括避免接触过敏原、药物治疗和免疫治疗等,但是部分患者治疗效果并不理想,究其原因主要与其发病机制复杂多样有关。细胞焦亡是程序性细胞死亡的一种,近年来研究表明细胞焦亡通过多种途径参与了AR的发生发展,部分药物可以通过抑制细胞焦亡来治疗AR。因此,深入探索细胞焦亡对AR的调控机制可能为AR的治疗提供新思路。论文就细胞焦亡在AR中的作用机制及研究进展进行综述。

关键词: 细胞焦亡, 变应性鼻炎, 炎症小体, caspase蛋白酶, NOD样受体蛋白

Abstract: Allergic rhinitis is an allergic inflammatory disease of the nasal mucosa caused by environmental and hereditary factors. The incidence rate of allergic rhinitis is increasing every year, and this has a serious impact on people's physical and mental health. The main therapeutic methods include drug therapy and immunotherapy, but the treatment effect is not ideal in some cases. The reason is mainly due to its complicated pathogenesis is complicated. Pyroptosis is a type of programmed cell death. In the recent years, studies have shown that pyroptosis is involved in the occurrence and development of allergic rhinitis. Some drugs can treat allergic rhinitis by inhibiting pyroptosis. Therefore, further exploration of the regulatory mechanisms of pyroptosis may provide new insights for the treatment of allergic rhinitis. This article reviews the mechanisms and research progress of pyroptosis in allergic rhinitis.

Key words: Pyroptosis, Allergic rhinitis, Inflammasome, Caspase, NLRP

中图分类号: 

  • R765
[1] Steelant B, Seys SF, van Gerven L, et al. Histamine and T helper cytokine-driven epithelial barrier dysfunction in allergic rhinitis[J]. J Allergy Clin Immunol, 2018, 141(3): 951-963.e8. doi:10.1016/j.jaci.2017.08.039.
[2] Bernstein DI, Schwartz G, Bernstein JA. Allergic rhinitis: mechanisms and treatment[J]. Immunol Allergy Clin North Am, 2016, 36(2): 261-278. doi:10.1016/j.iac.2015.12.004.
[3] Yang L, Fu JR, Zhou YF. Research progress in atopic March[J]. Front Immunol, 2020, 11: 1907. doi:10.3389/fimmu.2020.01907.
[4] 中华耳鼻咽喉头颈外科杂志编辑委员会鼻科组, 中华医学会耳鼻咽喉头颈外科学分会鼻科学组. 中国慢性鼻窦炎诊断和治疗指南(2018)[J]. 中华耳鼻咽喉头颈外科杂志, 2019, 54(2): 81-100. doi:10.3760/cma.j.issn.1673-0860.2019.02.001.
[5] Zissler UM, Esser-von Bieren J, Jakwerth CA, et al. Current and future biomarkers in allergic asthma[J]. Allergy, 2016, 71(4): 475-494. doi:10.1111/all.12828.
[6] Meng YF, Wang CS, Zhang L. Recent developments and highlights in allergic rhinitis[J]. Allergy, 2019, 74(12): 2320-2328. doi:10.1111/all.14067.
[7] Galluzzi L, Vitale I, Aaronson SA, et al. Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018[J]. Cell Death Differ, 2018, 25(3): 486-541. doi:10.1038/s41418-017-0012-4.
[8] 黄清宇, 杜楚江, 张雨竹, 等. 细胞焦亡研究进展[J]. 中国免疫学杂志, 2020, 36(2): 245-250. doi:10.3969/j.issn.1000-484X.2020.02.022. HUANG Qingyu, DU Chujiang, ZHANG Yuzhu, et al. Research progress of pyroptosis[J]. Cellular & Molecular Immunology, 2020, 36(2): 245-250. doi:10.3969/j.issn.1000-484X.2020.02.022.
[9] Liston A, Masters SL. Homeostasis-altering molecular processes as mechanisms of inflammasome activation[J]. Nat Rev Immunol, 2017, 17(3): 208-214. doi:10.1038/nri.2016.151.
[10] Rathinam VAK, Fitzgerald KA. Inflammasome complexes: emerging mechanisms and effector functions[J]. Cell, 2016, 165(4): 792-800. doi:10.1016/j.cell.2016.03.046.
[11] Man SM, Kanneganti TD. Regulation of inflammasome activation[J]. Immunol Rev, 2015, 265(1): 6-21. doi:10.1111/imr.12296.
[12] 魏亚宁, 仇惠莺. NLRP3炎症小体活化促进上皮细胞焦亡诱导变应性鼻炎[J]. 免疫学杂志, 2021, 37(2): 140-144. doi:10.13431/j.cnki.immunol.j.20210021. WEI Yaning, QIU Huiying. NLRP3 inflammasome activation promotes the development of allergic rhinitis via epithelium pyroptosis[J]. Immunological Journal, 2021, 37(2): 140-144. doi:10.13431/j.cnki.immunol.j.20210021.
[13] Liu X, Zhang ZB, Ruan JB, et al. Inflammasome-activated gasdermin D causes pyroptosis by forming membrane pores[J]. Nature, 2016, 535(7610): 153-158. doi:10.1038/nature18629.
[14] Shi JJ, Zhao Y, Wang K, et al. Cleavage of GSDMD by inflammatory caspases determines pyroptotic cell death[J]. Nature, 2015, 526(7575): 660-665. doi:10.1038/nature15514.
[15] Bergougnan C, Dittlein DC, Hümmer E, et al. Physical and immunological barrier of human primary nasal epithelial cells from non-allergic and allergic donors[J]. World Allergy Organ J, 2020, 13(3): 100109. doi:10.1016/j.waojou.2020.100109.
[16] Han MW, Kim SH, Oh I, et al. Serum IL-1β can be a biomarker in children with severe persistent allergic rhinitis[J]. Allergy Asthma Clin Immunol, 2019, 15: 58. doi:10.1186/s13223-019-0368-8.
[17] Sanders NL, Mishra A. Role of interleukin-18 in the pathophysiology of allergic diseases[J]. Cytokine Growth Factor Rev, 2016, 32: 31-39. doi:10.1016/j.cytogfr.2016.07.001.
[18] Man SM, Karki R, Kanneganti TD. Molecular mechanisms and functions of pyroptosis, inflammatory caspases and inflammasomes in infectious diseases[J]. Immunol Rev, 2017, 277(1): 61-75. doi:10.1111/imr.12534.
[19] Robinson N, Ganesan R, Heged s C, et al. Programmed necrotic cell death of macrophages: focus on pyroptosis, necroptosis, and parthanatos[J]. Redox Biol, 2019, 26: 101239. doi:10.1016/j.redox.2019.101239.
[20] Tibbitt CA, Stark JM, Martens L, et al. Single-cell RNA sequencing of the T helper cell response to house dust mites defines a distinct gene expression signature in airway Th2 cells[J]. Immunity, 2019, 51(1): 169-184.e5. doi:10.1016/j.immuni.2019.05.014.
[21] 杨斯迪, 邓奇峰, 黄瑞, 等. 炎性小体激活与细胞焦亡的研究进展[J]. 微生物与感染, 2017, 12(3): 192-196. doi:10.3969/j.issn.1673-6184.2017.03.010. YANG Sidi, DENG Qifeng, HUANG Rui, et al. Research progress on inflammasome activation and pyroptosis[J]. Journal of Microbes and Infections, 2017, 12(3): 192-196. doi:10.3969/j.issn.1673-6184.2017.03.010.
[22] Liu QY, Zhang DY, Hu DY, et al. The role of mitochondria in NLRP3 inflammasome activation[J]. Mol Immunol, 2018, 103: 115-124. doi:10.1016/j.molimm.2018.09.010.
[23] Yang ZX, Liang CQ, Wang TY, et al. NLRP3 inflammasome activation promotes the development of allergic rhinitis via epithelium pyroptosis[J]. Biochem Biophys Res Commun, 2020, 522(1): 61-67. doi:10.1016/j.bbrc.2019.11.031.
[24] Yu XF, Wang M, Zhao H, et al. Targeting a novel hsa_circ_0000520/miR-556-5p/NLRP3 pathway-mediated cell pyroptosis and inflammation attenuates ovalbumin(OVA)-induced allergic rhinitis(AR)in mice models[J]. Inflamm Res, 2021, 70(6): 719-729. doi:10.1007/s00011-021-01472-z.
[25] Zhuang J, Cui HY, Zhuang LL, et al. Bronchial epithelial pyroptosis promotes airway inflammation in a murine model of toluene diisocyanate-induced asthma[J]. Biomedecine Pharmacother, 2020, 125: 109925. doi:10.1016/j.biopha.2020.109925.
[26] Tenthorey JL, Chavez RA, Thompson TW, et al. NLRC4 inflammasome activation is NLRP3- and phosphorylation-independent during infection and does not protect from melanoma[J]. J Exp Med, 2020, 217(7): e20191736. doi:10.1084/jem.20191736.
[27] Li WB, Deng MH, Loughran PA, et al. LPS induces active HMGB1 release from hepatocytes into exosomes through the coordinated activities of TLR4 and caspase-11/GSDMD signaling[J]. Front Immunol, 2020, 11: 229. doi:10.3389/fimmu.2020.00229.
[28] Zas ona Z, Flis E, Wilk MM, et al. Caspase-11 promotes allergic airway inflammation[J]. Nat Commun, 2020, 11(1): 1055. doi:10.1038/s41467-020-14945-2.
[29] Tsukamoto H, Takeuchi S, Kubota K, et al. Lipopolysaccharide(LPS)-binding protein stimulates CD14-dependent Toll-like receptor 4 internalization and LPS-induced TBK1-IKK -IRF3 axis activation[J]. J Biol Chem, 2018, 293(26): 10186-10201. doi:10.1074/jbc.M117.796631.
[30] Hu M, Li XP, Zhang JL, et al. GEN-27 exhibits anti-inflammatory effects by suppressing the activation of NLRP3 inflammasome and NF-κB pathway[J]. Cell Biol Int, 2019, 43(10): 1184-1192. doi:10.1002/cbin.11101.
[31] Moreira-Souza ACA, Almeida-da-Silva CLC, Rangel TP, et al. The P2X7 receptor mediates Toxoplasma gondii control in macrophages through canonical NLRP3 inflammasome activation and reactive oxygen species production[J]. Front Immunol, 2017, 8: 1257. doi:10.3389/fimmu.2017.01257.
[32] Harcha PA, López X, Sáez PJ, et al. Pannexin-1 channels are essential for mast cell degranulation triggered during type I hypersensitivity reactions[J]. Front Immunol, 2019, 10: 2703. doi:10.3389/fimmu.2019.02703.
[33] Wang YP, Gao WQ, Shi XY, et al. Chemotherapy drugs induce pyroptosis through caspase-3 cleavage of a gasdermin[J]. Nature, 2017, 547(7661): 99-103. doi:10.1038/nature22393.
[34] Yu JH, Li S, Qi J, et al. Cleavage of GSDME by caspase-3 determines lobaplatin-induced pyroptosis in colon cancer cells[J]. Cell Death Dis, 2019, 10(3): 193. doi:10.1038/s41419-019-1441-4.
[35] Malireddi RKS, Gurung P, Mavuluri J, et al. TAK1 restricts spontaneous NLRP3 activation and cell death to control myeloid proliferation[J]. J Exp Med, 2018, 215(4): 1023-1034. doi:10.1084/jem.20171922.
[36] Orning P, Weng D, Starheim K, et al. Pathogen blockade of TAK1 triggers caspase-8-dependent cleavage of gasdermin D and cell death[J]. Science, 2018, 362(6418): 1064-1069. doi:10.1126/science.aau2818.
[37] Fritsch M, Günther SD, Schwarzer R, et al. Caspase-8 is the molecular switch for apoptosis, necroptosis and pyroptosis[J]. Nature, 2019, 575(7784): 683-687. doi:10.1038/s41586-019-1770-6.
[38] Mascarenhas DPA, Cerqueira DM, Pereira MSF, et al. Inhibition of caspase-1 or gasdermin-D enable caspase-8 activation in the Naip5/NLRC4/ASC inflammasome[J]. PLoS Pathog, 2017, 13(8): e1006502. doi:10.1371/journal.ppat.1006502.
[39] Schneider KS, Gro CJ, Dreier RF, et al. The inflammasome drives GSDMD-independent secondary pyroptosis and IL-1 release in the absence of caspase-1 protease activity[J]. Cell Rep, 2017, 21(13): 3846-3859. doi:10.1016/j.celrep.2017.12.018.
[40] Qi X, Gurung P, Malireddi RK, et al. Critical role of caspase-8-mediated IL-1 signaling in promoting Th2 responses during asthma pathogenesis[J]. Mucosal Immunol, 2017, 10(1): 128-138. doi:10.1038/mi.2016.25.
[41] Zhang WT, Ba GY, Tang R, et al. Ameliorative effect of selective NLRP3 inflammasome inhibitor MCC950 in an ovalbumin-induced allergic rhinitis murine model[J]. Int Immunopharmacol, 2020, 83: 106394. doi:10.1016/j.intimp.2020.106394.
[42] Xiao LF, Jiang L, Hu Q, et al. microRNA-133b ameliorates allergic inflammation and symptom in murine model of allergic rhinitis by targeting Nlrp3[J]. Cell Physiol Biochem, 2017, 42(3): 901-912. doi:10.1159/000478645.
[43] Huang Y, Jiang H, Chen Y, et al. Tranilast directly targets NLRP3 to treat inflammasome-driven diseases[J]. EMBO Mol Med, 2018, 10(4): e8689. doi:10.15252/emmm.201708689.
[44] Kato A. Group 2 innate lymphoid cells in airway diseases[J]. Chest, 2019, 156(1): 141-149. doi:10.1016/j.chest.2019.04.101.
[45] Hu WX, Zhou WY, Zhu XL, et al. Anti-interleukin-1 beta/tumor necrosis factor-alpha IgY antibodies reduce pathological allergic responses in Guinea pigs with allergic rhinitis[J]. Mediators Inflamm, 2016, 2016: 3128182. doi:10.1155/2016/3128182.
[46] Li DD, Ren WY, Jiang ZL, et al. Regulation of the NLRP3 inflammasome and macrophage pyroptosis by the p38 MAPK signaling pathway in a mouse model of acute lung injury[J]. Mol Med Rep, 2018, 18(5): 4399-4409. doi:10.3892/mmr.2018.9427.
[47] Liu ZJ, Gan L, Xu YT, et al. Melatonin alleviates inflammasome-induced pyroptosis through inhibiting NF-κB/GSDMD signal in mice adipose tissue[J]. J Pineal Res, 2017, 63(1):e12414. doi:10.1111/jpi.12414.
[48] Aye A, Song YJ, Jeon YD, et al. Xanthone suppresses allergic contact dermatitis in vitro and in vivo[J]. Int Immunopharmacol, 2020, 78: 106061. doi:10.1016/j.intimp.2019.106061.
[49] Wang GH, Cheng N. Paeoniflorin inhibits mast cell-mediated allergic inflammation in allergic rhinitis[J]. J Cell Biochem, 2018, 119(10): 8636-8642. doi:10.1002/jcb.27135.
[50] Hu HL, Li HX. Prunetin inhibits lipopolysaccharide-induced inflammatory cytokine production and MUC5AC expression by inactivating the TLR4/MyD88 pathway in human nasal epithelial cells[J]. Biomed Pharmacother, 2018, 106: 1469-1477. doi:10.1016/j.biopha.2018.07.093.
[51] Van Nguyen T, Piao CH, Fan YJ, et al. Anti-allergic rhinitis activity of α-lipoic acid via balancing Th17/Treg expression and enhancing Nrf2/HO-1 pathway signaling[J]. Sci Rep, 2020, 10(1): 12528. doi:10.1038/s41598-020-69234-1.
[52] Fu M, Fu SL, Ni SH, et al. Anti-inflammatory effect of epigallocatechin gallate in a mouse model of ovalbumin-induced allergic rhinitis[J]. Int Immunopharmacol, 2017, 49: 102-108. doi:10.1016/j.intimp.2017.05.030.
[53] 颜亮, 李陈广, 徐丽慧, 等. 黄芩苷对NLRP3炎症小体活化和细胞焦亡的抑制作用及其机制研究[J]. 免疫学杂志, 2018, 34(2): 93-100,114. doi:10.13431/j.cnki.immunol.j.20180014. YAN Liang, LI Chenguang, XU Lihui, et al. Inhibitory effects of baicalin on NLRP3 inflammasome activation and pyroptosis and the underlying mechanism[J]. Immunological Journal, 2018, 34(2): 93-100, 114. doi:10.13431/j.cnki.immunol.j.20180014.
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