Expression of IL-17 and syndecan-1 in nasal polyps and their correlation with nasal polyps

Abstract

Nasal polyp (NP) is a common chronic inflammatory disease of the nasal cavity and sinuses. Although some authors have suggested that NP is related to inflammatory factors such as interleukin (IL)-1β, IL-5, IL-8, granulocyte-macrophage colony-stimulating factor (GM-CSF), tumor necrosis factor (TNF)-α, and IL-17, the mechanisms underlying the pathogenesis and progression of NP remain obscure. This study investigated the expression and distribution of IL-17 and syndecan-1 in NP, and explored the roles of these two molecules in the pathogenesis of eosinophilic chronic rhinosinusitis with nasal polyps (Eos CRSwNP) and non-Eos CRSwNP. Real-time PCR and immunohistochemistry were used to detect the expression of IL-17 and syndecan-1 in samples [NP, unciform process (UP) from patients with CRS, and middle turbinate (MT) from healthy controls undergoing pituitary tumor surgery]. The results showed that the expression levels of IL-17 and syndecan-1 were upregulated in both NP and UP tissues, but both factors were higher in NP tissues than in UP tissues. There was no significant difference in IL-17 levels between the Eos CRSwNP and non-Eos CRSwNP samples, and syndecan-1 levels were increased in the non-Eos CRSwNP tissues as compared with those in Eos CRSwNP tissues. In all of the groups, there was a close correlation between the expression of IL-17 and syndecan-1 in nasal mucosa epithelial cells, glandular epithelial cells, and inflammatory cells, suggesting that IL-17 and syndecan-1 may play a role, and interact with each other, in the pathogenesis of non-Eos CRSwNP.

Keywords

interleukin-17 / syndecan-1 / nasal polyps

References

[1] ShinSH, YeMK, KimJK, et al. . Histological characteristics of chronic rhinosinusitis with nasal polyps: Recent 10-year experience of a single center in Daegu, Korea. Am J Rhinol Allergy, 2014, 28(2): 95-98 PMID: 24717942

[2] XuJ, HanR, WooKD, et al. . Role of interleukin-10 on nasal polypogenesis in patients with chronic rhinosinusitis with nasal polyps. Plos One, 2016, 11(9): 1-21

[3] ChengYS, BleierBS. Influence of P-glycoprotein function on chronic rhinosinusitis/nasal polyps pathophysiology. Adv Otorhinolaryngol, 2016, 79: 38-47 PMID: 27466845

[4] OnerciM, ElsurerC, GuzelEE, et al. . Distribution of inflammatory cells, adhesion molecules, intermediate filaments, and chemokine receptors in subgroups of nasal polyp patients. Am J Rhinol Allergy, 2011, 25(5): 176

[5] SaitohT, KusunokiT, YaoT, et al. . Role of interleukin-17A in the eosinophil accumulation and mucosal remodeling in chronic rhinosinusitis with nasal polyps associated with asthma. Int Arch Allergy Immunol, 2010, 151: 8-16 PMID: 19672092

[6] FokkensWJ, LundVJ, MullolJ, et al. . European position paper on rhinosinusitis and nasal polyps 2012. Rhinol Suppl, 2012, 3(23): 1-298

[7] MehrotraP, CollettJA, MckinneyS, et al. . IL-17 mediates neutrophil infiltration and renal fibrosis following recovery from ischemia reperfusion: compensatory role of natural killer cells in athymic rats. Am J Physiol-Renal, 2017, 312(3): F385-F397

[8] MccarthyMK, ZhuL, ProcarioMC, et al. . IL-17 contributes to neutrophil recruitment but not to control of viral replication during acute mouse adenovirus type 1 respiratory infection. Virology, 2014, 456-457(1): 259-267 PMID: 24889245

[9] BrodlieM, McKeanMC, JohnsonGE, et al. . Raised interleukin-17 is immunolocalised to neutrophils in cystic fibrosis lung disease. Eur Respir J, 2011, 37(6): 1378-1385 PMID: 21109552

[10] CurtisMM, WaySS. Interleukin-17 in host defence against bacterial, mycobacterial and fungal pathogens. Immunology, 2009, 126: 177-185 PMID: 19125888 PMCID: 2632692

[11] BrauerR, GeL, SchlesingerSY, et al. . Syndecan-1 attenuates lung injury during influenza infection by potentiating c-met signaling to suppress epithelial apoptosis. Am J Resp Crit Care, 2016, 194(3): 1-55

[12] GharbaranR. Advances in the molecular functions of syndecan-1 (SDC1/CD138) in the pathogenesis of malignancies. Crit Rev Oncol Hemat, 2015, 94(1): 1-17

[13] AbuEAA, NawazMI, MohammadG, et al. . Upregulated expression of heparanase in the vitreous of patients with proliferative diabetic retinopathy originates from activated endothelial cells and leukocytes. Invest Ophth Vis Sci, 2015, 56(13): 8239-8247

[14] YuanK, HongTM, ChenJJ, et al. . Syndecan-1 up-regulated by ephrinB2/EphB4 plays dual roles in inflammatory angiogenesis. Blood, 2004, 104(4): 1025-1033 PMID: 15126321

[15] DerksenPW, de GorterDJ, MeijerHP, et al. . The hepatocyte growth factor/Met pathway controls proliferation and apoptosis in multiple myeloma. Leukemia, 2003, 17(4): 764-774 PMID: 12682635

[16] ParkPW, ReizesO, BernfieldM. Cell surface heparan sulfate proteoglycans: selective regulators of ligand-receptor encounters. J Biol Chem, 2000, 275(39): 29923-29926 PMID: 10931855

[17] WangZ, GötteM, BernfieldM, et al. . Constitutive and accelerated shedding of murine syndecan-1 is mediated by cleavage of its core protein at a specific juxtamembrane site. Biochemistry-US, 2005, 44(37): 12355-12361

[18] SteppanJ, HoferS, FunkeB, et al. . Sepsis and major abdominal surgery lead to flaking of the endothelial glycocalix. J Surg Res, 2011, 165(1): 136-141 PMID: 19560161

[19] HenrichM, GrussM, WeigandMA, et al. . Sepsis-induced degradation of endothelial glycocalix. Sci World J, 2010, 10: 917-923

[20] JiaoJ, DuanS, MengN, et al. . Role of IFN-?, IL-13 and IL-17 on mucociliary differentiation of nasal epithelial cells in chronic rhinosinusitis with nasal polyps. Clin Exp Allergy, 2016, 46(3): 449-460 PMID: 26399381

[21] NiuYZ, GongG S, ChenS, et al. . Effects of IL-17 on expression of GRO-a and IL-8 in fibroblasts from nasal polyps. J Huazhong Univ Sci Technolog Med Sci, 2014, 34(4): 591-595 PMID: 25135733

[22] MurphyDM, ForrestIA, CorrisPA, et al. . Simvastatin attenuates release of neutrophilic and remodeling factors from primary bronchial epithelial cells derived from stable lung transplant recipients. Am J Physiol Lung Cell Mol Physiol, 2008, 294: L592-L599 PMID: 18203812

[23] MarshallLJ, RamdinLS, BrooksT, et al. . Plasminogen activator inhibitor-1 supports IL-8-mediated neutrophil transendothelial migration by inhibition of the constitutive shedding of endothelial IL-8/heparan sulfate/ syndecan-1 complexes. J Immunol, 2003, 171(4): 2057-2065 PMID: 12902511

[24] KollsJK, LindénA. Interleukin-17 family members and inflammation. Immunity, 2004, 21(4): 467-476 PMID: 15485625

[25] LindénA. Role of interleukin-17 and the neutrophil in asthma. Int Arch Allergy Immunol, 2001, 126(3): 179-184 PMID: 11752873

[26] CaoPP, LiHB, WangBF, et al. . Distinct immunopathologic characteristics of various types of chronic rhinosinusitis in adult Chinese. J Allergy Clin Immunol, 2009, 124(3): 1-2

[27] JiangXD, LiGY, LiL, et al. . The characterization of IL-17A expression in patients with chronic rhinosinusitis with nasal polyps. Am J Rhinol Allergy, 2011, 25(5): 171-175

[28] KönigK, KlemensC, HaackM, et al. . Cytokine patterns in nasal secretion of non-atopic patients distinguish between chronic rhinosinusitis with or without nasal polyps. Allergy Asthma Clin Immunol, 2016, 12: 19 PMID: 27127525 PMCID: 4849093

[29] HuXD, BaoYY, ZhouSH, et al. . Interleukin-17A expression in patients with chronic rhinosinusitis and its relationship with clinical features. J Int Med Res, 2013, 41(3): 777-784 PMID: 23613503

[30] BabaS, KagoyaR, KondoK, et al. . T-cell phenotypes in chronic rhinosinusitis with nasal polyps in Japanese patients. Allergy Asthma Clin Immunol, 2015, 11: 33 PMID: 26594227 PMCID: 4653844

[31] VenkatesanN, LavigneP, LavigneF, et al. . Effects of fluticasone furoate on clinical and immunological outcomes (IL-17) for patients with nasal polyposis naive to steroid treatment. Ann Oto Rhinol Laryn, 2016, 125(3): 213-218

[32] ReynoldsJM, AngkasekwinaiP, DongC. IL-17 family member cytokines: Regulation and function in innate immunity. Cytokine Growth Factor Rev, 2010, 21(6): 413-423 PMID: 21074482 PMCID: 3008409

[33] CuaDJ, TatoCM. Innate IL-17-producing cells: the sentinels of the immune system. Nat Rev Immunol, 2010, 10(7): 479-490 PMID: 20559326

[34] Van ZeleT, ClaeysS, GevaertP, et al. . Differentiation of chronic sinus diseases by measurement of inflammatory mediators. Allergy, 2006, 61(11): 1280-1289 PMID: 17002703

[35] KimDY, LeeSH, CarterRG, et al. . A recently established murine model of nasal polyps demonstrates activation of B cells, as occurs in human nasal polyps. Am J Respir Cell Mol, 2016, 55(2): 170-175

[36] GoK, IshinoT, NakashimoY, et al. . Analysis of syndecan-1 and TGF-beta expression in the nasal mucosa and nasal polyps. Auris Nasus Larynx, 2010, 37(4): 427-435 PMID: 20047808

[37] SzatmáriT, MundtF, HeidarihamedaniG, et al. . Novel genes and pathways modulated by syndecan-1: implications for the proliferation and cell-cycle regulation of malignant mesothelioma cells. Plos One, 2012, 7(10): 48091

[38] TengYH, AquinoRS, ParkPW. Molecular functions of syndecan-1 in disease. Matrix Biol, 2012, 31(1): 3-16 PMID: 22033227

[39] van den BergA, KuiperM, SnoekM, et al. . Interleukin-17 induces hyperresponsive interleukin-8 and interleukin-6 production to tumor necrosis factor-alpha in structural lung cells. Am J Respir Cell Mol Biol, 2005, 33(1): 97-104 PMID: 15845864

[40] MoletSM, HamidQA, HamilosDL. IL-11 and IL-17 expression in nasal polyps: relationship to collagen deposition and suppression by intranasal fluticasone propionate. Laryngoscope, 2003, 113(10): 1803-1812 PMID: 14520110