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Abstract: Nasal polyps, as a subtype of chronic sinusitis, is prone to clinical recurrence and seriously affects the quality of life of patients, but its pathogenesis is unclear. It is considered to be a chronic inflammation of the nasal-sinus mucosa under the combined action of multiple factors. Among them, nasal mucosal epithelial injury and shedding are the main pathological features. Nasal-sinus epithelial separated nasal sinuses with the outside world, is the complex natural biological barrier to resist external stimuli and the key to maintaining homeostasis in the nasal sinuses. At present, the epithelium is considered not only as a "target organ" but also as an "effector" and a central regulator of the inflammatory response. This paper reviews the role of epithelial cells in the formation and development of nasal polyps, including the epithelial cell layer were stimulated not only leads to tissue remodeling, changes in mucociliary clearance, abnormal ion channels, and proliferation and apoptosis imbalance, but also produce a series of bioactive substances in response to various internal and external stimuli.Therefore, maintaining the integrity of the structure and function of airway mucosal epithelial cells may be a new approach for clinical prevention and treatment of nasal polyps.
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Key words:
- nasal polyps /
- cell of epithelial tissue /
- target organ /
- effector
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[1] Zhang N, Van Crombruggen K, Gevaert E, et al. Barrier function of the nasal mucosa in health and type-2 biased airway diseases[J]. Allergy, 2016, 71(3): 295-307. doi: 10.1111/all.12809
[2] Pacova H, Astl J, Martinek J. The pathogenesis of chronic inflammation and malignant transformation in the human upper airways: the role of beta-defensins, eNOS, cell proliferation and apoptosis[J]. Histol Histopathol, 2009, 24(7): 815-820.
[3] Hirschberg A, Kiss M, Kadocsa E, et al. Different activations of toll-like receptors and antimicrobial peptides in chronic rhinosinusitis with or without nasal polyposis[J]. Eur Arch Otorhinolaryngol, 2016, 273(7): 1779-1788. doi: 10.1007/s00405-015-3816-1
[4] Kim JH, Park BL, Cheong HS, et al. HLA-DRA polymorphisms associated with risk of nasal polyposis in asthmatic patients[J]. Am J Rhinol Allergy, 2012, 26(1): 12-17. doi: 10.2500/ajra.2012.26.3692
[5] Khalmuratova R, Park JW, Shin HW. Immune Cell Responses and Mucosal Barrier Disruptions in Chronic Rhinosinusitis[J]. Immune Netw, 2017, 17(1): 60-67. doi: 10.4110/in.2017.17.1.60
[6] Azizzadeh Delshad A, Jalali Nadoushan M, Davati A, et al. Expression of Vascular Endothelial Growth Factor in Nasal Polyp and Chronic Rhinosinusitis[J]. Iran J Pathol, 2016, 11(3): 231-237.
[7] Muluk NB, Arikan OK, Atasoy P, et al. Inducible nitric oxide synthase(iNOS)in sinonasal polyp pathogenesis[J]. B-ENT, 2013, 9(3): 207-216.
[8] Lin H, Lin D, Xiong XS, et al. Role of platelet-derived growth factor-α in eosinophilic and non-eosinophilic chronic rhinosinusitis with nasal polyps[J]. Int Forum Allergy Rhinol, 2014, 4(11): 909-914. doi: 10.1002/alr.21419
[9] 罗庆, 朱恒涛, 冯琨, 等. 慢性鼻-鼻窦炎中缺氧诱导因子1α的表达及与黏蛋白分泌的关系[J]. 中华耳鼻咽喉头颈外科杂志, 2015, 50(2): 138-144. doi: 10.3760/cma.j.issn.1673-0860.2015.02.010
[10] Wu YS, Jiang J, Ahmadi S, et al. ORKAMBI-Mediated Rescue of Mucociliary Clearance in Cystic Fibrosis Primary Respiratory Cultures Is Enhanced by Arginine Uptake, Arginase Inhibition, and Promotion of Nitric Oxide Signaling to the Cystic Fibrosis Transmembrane Conductance Regulator Channel[J]. Mol Pharmacol, 2019, 96(4): 515-525. doi: 10.1124/mol.119.117143
[11] Koennecke M, Benecke F, Masche A, et al. Increased phosphorylation of eNOS in nasal polyps of chronic rhinosinusitis patients can be diminished by 1, 8-cineol[J]. Nitric Oxide, 2018, 78: 89-94. doi: 10.1016/j.niox.2018.06.002
[12] Jiang Y, Xu J, Chen Y, et al. Expression and distribution of epithelial sodium channel in nasal polyp and nasal mucosa[J]. Eur Arch Otorhinolaryngol, 2015, 272(11): 3361-3366. doi: 10.1007/s00405-014-3477-5
[13] Shikani AH, Sidhaye VK, Basaraba RJ, et al. Mucosal expression of aquaporin 5 and epithelial barrier proteins in chronic rhinosinusitis with and without nasal polyps[J]. Am J Otolaryngol, 2014, 35(3): 377-383. doi: 10.1016/j.amjoto.2013.11.011
[14] Frauenfelder C, Woods C, Hussey D, et al. Aquaporin expression profiles in normal sinonasal mucosa and chronic rhinosinusitis[J]. Int Forum Allergy Rhinol, 2014, 4(11): 901-908. doi: 10.1002/alr.21415
[15] Mumbuc S, Karakok M, Baglam T, et al. Immunohistochemical analysis of PCNA, Ki67 and p53 in nasal polyposis and sinonasal inverted papillomas[J]. J Int Med Res, 2007, 35(2): 237-241. doi: 10.1177/147323000703500208
[16] Heo KW, Park SK, Lee YM, et al. Methotrexate Induces Apoptosis in Organ-Cultured Nasal Polyps Via the Fas Pathway[J]. J Craniofac Surg, 2017, 28(3): 806-809. doi: 10.1097/SCS.0000000000003562
[17] 陈丹, 陈璐, 肖玲, 等. 鼻息肉中抑癌基因及增殖凋亡基因研究进展[J]. 临床耳鼻咽喉头颈外科杂志, 2015, 29(23): 2099-2102. https://www.cnki.com.cn/Article/CJFDTOTAL-LCEH201523025.htm
[18] Wynne M, Atkinson C, Schlosser RJ, et al. Contribution of Epithelial Cell Dysfunction to the Pathogenesis of Chronic Rhinosinusitis with Nasal Polyps[J]. Am J Rhinol Allergy, 2019, 33(6): 782-790. doi: 10.1177/1945892419868588
[19] Yamada T, Miyabe Y, Ueki S, et al. Eotaxin-3 as a Plasma Biomarker for Mucosal Eosinophil Infiltration in Chronic Rhinosinusitis[J]. Front Immunol, 2019, 10: 74-74. doi: 10.3389/fimmu.2019.00074
[20] Li J, Jiao J, Wang M, et al. Hypomethylation of the IL8 promoter in nasal epithelial cells of patients with chronic rhinosinusitis with nasal polyps[J]. J Allergy Clin Immunol, 2019, 144(4): 993-1003. e12. doi: 10.1016/j.jaci.2019.06.042
[21] Huriyati E, Darwin E, Yanwirasti Y, et al. Differences in Expression of Inflammatory Mediator in Mucosal and Polyp Tissue between Chronic Rhinosinusitis and Recurrent Chronic Rhinosinusitis[J]. Open Access Maced J Med Sci, 2019, 7(11): 1733-1738. doi: 10.3889/oamjms.2019.341
[22] Khalmuratova R, Lee M, Mo JH, et al. Wogonin attenuates nasal polyp formation by inducing eosinophil apoptosis through HIF-1α and survivin suppression[J]. Sci Rep, 2018, 8(1): 6201-6201. doi: 10.1038/s41598-018-24356-5
[23] 丁楠, 李春苗, 巴云鹏. PLUNC、TLR2及NF-κB在鼻息肉组织中的表达及意义[J]. 临床耳鼻咽喉头颈外科杂志, 2017, 31(2): 130-134. https://www.cnki.com.cn/Article/CJFDTOTAL-LCEH201702013.htm
[24] Ahmadzada S, Ende JA, Alvarado R, et al. Responses of Well-differentiated Human Sinonasal Epithelial Cells to Allergen Exposure and Environmental Pollution in Chronic Rhinosinusitis[J]. Am J Rhinol Allergy, 2019, 33(6): 624-633. doi: 10.1177/1945892419853103
[25] Zheng R, Wang D, Wang K, et al. Elevated expression of IL-17RB and ST2 on myeloid dendritic cells is associated with a Th2-skewed eosinophilic inflammation in nasal polyps[J]. Clin Transl Allergy, 2018, 8: 50-50. doi: 10.1186/s13601-018-0237-4
[26] Weller PF, Spencer LA. Functions of tissue-resident eosinophils[J]. Nat Rev Immunol, 2017, 17(12): 746-760. doi: 10.1038/nri.2017.95
[27] 孙雪芳. BAFF在嗜酸粒细胞及中性粒细胞为主型的伴有鼻息肉的慢性鼻窦炎中发病机制的相关研究[J]. 临床耳鼻咽喉头颈外科杂志, 2019, 33(2): 183-186. https://www.cnki.com.cn/Article/CJFDTOTAL-LCEH201902023.htm
[28] 高雅丽, 王威清, 朱真真, 等. 趋化因子在嗜酸性慢性鼻-鼻窦炎伴鼻息肉中的价值研究[J]. 临床耳鼻咽喉头颈外科杂志, 2017, 31(18): 1458-1461. https://www.cnki.com.cn/Article/CJFDTOTAL-LCEH201718024.htm
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