YKL-40与慢性鼻-鼻窦炎组织重构的相关性探讨

doi:10.6040/j.issn.1673-3770.0.2017.214

摘要/Abstract

摘要： YKL-40是哺乳类动物类几丁质酶蛋白家族的一员。近年来的多项研究则进一步表明YKL-40在哮喘、关节炎等多种炎性疾病中表达升高,并在疾病的组织重塑中发挥了重要作用。慢性鼻-鼻窦炎(CRS)是鼻-鼻窦黏膜的持续性炎症,主要表现为鼻塞、黏性分泌物、鼻黏膜充血和后鼻滴漏,次要表现为面部压迫感和头痛。CRS的发病机制十分复杂,目前已知炎性反应和组织重构在病理进程中发挥重要作用。在CRS临床分型、诊断和治疗等诸多方面尚存在争议,目前临床上主要依靠鼻内镜检查及CT扫描进行分型诊断,缺乏能在病理生理机制及分子细胞水平深入反映疾病特征的标志物。结合文献探讨YKL-40与慢性鼻窦炎组织重构和炎性反应的相关性以及作为血清标志物的可能性。

关键词: 慢性鼻窦炎, 组织重构, 炎性反应, YKL-40

Abstract: YKL-40 is a member of the mammalian chitinase proteins family, also known as chitinase 3-like 1 or cartilage glycoprotein 39. In recent years, several studies have demonstrated that YKL-40 is highly expressed in many inflammatory diseases such as asthma, arthritis, and tissue remodeling disease. Chronic rhinosinusitis(CRS)is a persistent inflammation that manifests as nasal congestion, viscous secretions, nasal mucosal hyperemia, and posterior nasal drip, with secondary manifestations of facial pressure and headache. The pathogenesis of CRS is complicated. Inflammatory reactions and tissue remodeling are known to play important roles in the pathological processes of CRS. CRS is controversial in many aspects, such as classification, diagnosis, and treatment. At present, classification mainly depends on clinical diagnosis using, for example, nasal endoscopic examination and computed tomography. No biomarkers that reflect the pathophysiology and characteristics of CRS have been found. This study investigated the correlation of YKL-40 expression with tissue remodeling and the inflammatory reactions in CRS, and the possibility of using YKL-40 as a serum marker.

Key words: Inflammatory reaction, Chronic rhino-sinusitis, YKL-40, Tissue remodel

中图分类号:

R765.4

乔叔芬,杨飞轮,王臻妮,李学忠. YKL-40与慢性鼻-鼻窦炎组织重构的相关性探讨[J]. 山东大学耳鼻喉眼学报, 2018, 32(4): 95-99.

QIAO Shufen, YANG Feilun, WANG Zhenni, LI Xuezhong. Relationship between YKL-40 and chronic rhinosinusitis[J]. J Otolaryngol Ophthalmol Shandong Univ, 2018, 32(4): 95-99.

参考文献

[1] Gliklich RE,Metson R. The health impact of chronic sinusitis in patients seeking otolaryngologic care[J]. Otolaryngol Head Neck Surg, 1995, 113(1):104-109.
[2] Hastan D, Fokkens WJ, Bachert C, et al. Chronic rhinosinusitis in Europe—an underestimated disease. A GA² LEN study[J]. Allergy, 2011, 66(9):1216-1223.
[3] Fokkens W, Lund V, Mullol J. European position paper on rhinosinusitis and nasal polyps 2007[J]. Rhinol Suppl, 2007, 45(20):1-136.
[4] 娄鸿飞,王成硕. 慢性鼻窦炎分型研究进展[J]. 山东大学耳鼻喉眼学报,2018,32(3):10-13. LOU Hongfei, WANG Chengshuo. Progress in classification of chronic sinusitis[J]. J Otolaryngol Ophthalmol Shandong Univ, 2018, 32(3):10-13.
[5] Zhang N, Van ZT, Perez-Novo C, et al. Different types of T-effector cells orchestrate mucosal inflammation in chronic sinus disease[J]. J Allergy Clin Immunol, 2008, 122(5):961-968.
[6] Shao R, Taylor SL, Oh DS, et al. Vascular heterogeneity and targeting: the role of YKL-40 in glioblastoma vascularization[J]. Oncotarget, 2015, 6(38):40507-40518.
[7] Rehli M, Krause SW, Andreesen R. Molecular characterization of the gene for human cartilage gp-39(CHI3L1), a member of the chitinase protein family and marker for late stages of macrophage differentiation[J]. Genomics, 1997, 43(2):221-225.
[8] Henrissat B, Davies G. Structural and sequence-based classification of glycoside hydrolases[J]. Curr Opin Struct Biol, 1997, 7(5):637-644.
[9] Johansen JS, Williamson MK, Rice JS, et al. Identification of proteins secreted by human osteoblastic cells in culture[J]. J Bone Miner Res, 1992, 7(5):501-512.
[10] Johansen JS, Jensen BV, Roslind A, et al. Serum YKL-40, a new prognostic biomarker in cancer patients?[J]. Cancer Epidemiol Biomarkers Prev, 2006, 15(2):194-202.
[11] Rathcke CN, Johansen JS, Vestergaard H. YKL-40, a biomarker of inflammation, is elevated in patients with type 2 diabetes and is related to insulin resistance[J]. Inflamm Res, 2006, 55(2):53-59.
[12] De CF, Gaufillier S, Bonnaud A, et al. YKL-40(cartilage gp-39)induces proliferative events in cultured chondrocytes and synoviocytes and increases glycosaminoglycan synthesis in chondrocytes[J]. Biochem Biophys Res Commun, 2001, 285(4):926-931.
[13] Recklies AD, White C, Ling H. The chitinase 3-like protein human cartilage glycoprotein 39(HC-gp39)stimulates proliferation of human connective-tissue cells and activates both extracellular signal-regulated kinase- and protein kinase B-mediated signalling pathways[J]. Biochem J, 2002, 365(1):119-126.
[14] Shackelton LM, Mann DM, Millis AJ. Identification of a 38-kDa heparin-binding glycoprotein(gp38k)in differentiating vascular smooth muscle cells as a member of a group of proteins associated with tissue remodeling[J]. J Biol Chem, 1995, 270(22):13076-13083.
[15] Malinda KM, Ponce L, Kleinman HK, et al. Gp38k, a protein synthesized by vascular smooth muscle cells, stimulates directional migration of human umbilical vein endothelial cells[J]. Exp Cell Res, 1999, 250(1):168-173.
[16] Millis AJ, Hoyle M, Reich E, et al. Isolation and characterization of a Mr = 38, 000 protein from differentiating smooth muscle cells[J]. J Biol Chem, 1985, 260(6):3754-3761.
[17] Väänänen T, Koskinen A, Paukkeri EL, et al. YKL-40 as a novel factor associated with inflammation and catabolic mechanisms in osteoarthritic joints[J]. Mediators Inflamm, 2014:215140. DOI:10.1155/2014/25140.
[18] Kazakova M, Batalov A, Deneva T, et al. Relationship between sonographic parameters and YKL-40 levels in rheumatoid arthritis[J]. Rheumatol Int, 2013, 33(2):341-346.
[19] Mukherjee R. Fire in the “hall”! Myocardial inflammation and recurrence of atrial fibrillation[J]. J Thorac Cardiovasc Surg, 2016, 151(6):1683-1685.
[20] Rathcke CN, Vestergaard H. YKL-40, a new inflammatory marker with relation to insulin resistance and with a role in endothelial dysfunction and atherosclerosis[J]. Inflamm Res, 2006, 55(6):221-227.
[21] Kucur M, Isman FK, Karadag B, et al. Serum YKL-40 levels in patients with coronary artery disease[J]. Coron Artery Dis, 2007, 18(5):391-396.
[22] Junker N, Johansen JS, Andersen CB, et al. Expression of YKL-40 by peritumoral macrophages in human small cell lung cancer[J]. Lung Cancer, 2005, 48(2):223-231.
[23] Li X, Meng J, Qiao X, et al. Expression of TGF, matrix metalloproteinases, and tissue inhibitors in Chinese chronic rhinosinusitis[J]. J Allergy Clin Immunol, 2010, 125(5):1061-1068.
[24] Bai TR, Knight DA. Structural changes in the airways in asthma: observations and consequences[J]. Clin Sci(Lond), 2005, 108(6):463-477.
[25] Salazar LM, Herrera AM. Fibrotic Response of Tissue Remodeling in COPD[J]. Lung, 2011, 189(2):101-109.
[26] Chupp GL, Lee CG, Jarjour N, et al. A chitinase-like protein in the lung and circulation of patients with severe asthma[J]. N Engl J Med, 2007, 357(20):2016-2027.
[27] Shuhui L, Mok YK, Wong WSF. Role of mammalian chitinases in asthma[J]. Int Arch Allergy Immunol, 2009, 149(4):369-377.
[28] Lai T, Wu D, Chen M, et al. YKL-40 expression in chronic obstructive pulmonary disease: relation to acute exacerbations and airway remodeling[J]. Respir Res, 2016, 17(1):31.
[29] Gumus A, Kayhan S, Cinarka H, et al. High serum YKL-40 level in patients with COPD is related to hypoxemia and disease severity[J]. Tohoku J Exp Med, 2013, 229(2):163-170.
[30] 陈思, 孙丽平, 丁利忠, 等. 与哮喘气道重塑相关的神经信号转导通路研究进展[J]. 中国中西医结合儿科学, 2015, 7(4):320-322. CHEN Si, SUN Liping, DING Lizhong, et al. Development of neural signal transduction pathway associated with airway remodeling of asthma[J]. Chin Pediatr Integr Tradit West Med, 2015, 7(4):320-322.
[31] Chen G, Khalil N. TGF-β1 increases proliferation of airway smooth muscle cells by phosphorylation of map kinases[J]. Respir Res, 2006, 7(1):2.
[32] Undevia NS, Dorscheid DR, Marroquin BA, et al. Smad and p38-MAPK signaling mediates apoptotic effects of transforming growth factor-beta1 in human airway epithelial cells[J]. Am J Physiol Lung Cell Mol Physiol, 2004, 287(3):515-524.
[33] Leivonen SK, Häkkinen L, Liu D, et al. Smad3 and extracellular signal-regulated kinase 1/2 coordinately mediate transforming growth factor-beta-induced expression of connective tissue growth factor in human fibroblasts[J]. J Invest Dermatol, 2005, 124(6):1162-1169.
[34] Tang H, Sun Y, Shi Z, et al. YKL-40 induces IL-8 expression from bronchial epithelium via MAPK(JNK and ERK)and NF-κB pathways, causing bronchial smooth muscle proliferation and migration[J]. J Immunol, 2013, 190(1):438-446.
[35] Van ZT, Claeys S, Gevaert P, et al. Differentiation of chronic sinus diseases by measurement of inflammatory mediators[J]. Allergy, 2006, 61(11):1280-1289.
[36] Van BN, Péreznovo CA, Basinski TM, et al. T-cell regulation in chronic paranasal sinus disease[J]. J Allergy Clin Immunol, 2008, 121(6):1435-1441.
[37] 李华斌, 赖玉婷. 慢性鼻-鼻窦炎的发病机制及诊疗进展[J]. 山东大学耳鼻喉眼学报, 2018, 32(3):4-9. LI Huabin, LAI Yuting. Pathogenesis, diagnosis, and treatment of chronic rhinosinusitis[J]. J Otolaryngol Ophthalmol Shandong Univ, 2018, 32(3):4-9.
[38] Van BN, Derycke L, Perez-Novo CA, et al. TGF-beta signaling and collagen deposition in chronic rhinosinusitis[J]. J Allergy Clin Immunol, 2009, 124(2):253-259.
[39] 马越, 吴帅, 蔡晓岚, 等. 类几丁质酶YKL-40及Toll样受体4在慢性鼻-鼻窦炎伴鼻息肉与不伴鼻息肉患者中表达的差异[J]. 中华耳鼻咽喉头颈外科杂志, 2015, 50(4):300-305. MA Yue, WU Shuai, CAI Xiaolan, et al. Expression of YKL-40 and TLR4 in patients with chronic rhinosinusitis[J]. Chin J Otorhinolaryngol Head Neck Surg, 2015, 50(4):300-305.

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