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Increased expression of the epithelial anion transporter pendrin/SLC26A4 in nasal polyps of patients with chronic rhinosinusitis

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单位: [1]Northwestern Univ, Div Allergy & Immunol, Feinberg Sch Med, Chicago, IL 60611 USA [2]Northwestern Univ, Dept Otolaryngol Head & Neck Surg, Feinberg Sch Med, Chicago, IL 60611 USA [3]Northwestern Univ, Div Endocrinol Metab & Mol Med, Feinberg Sch Med, Chicago, IL 60611 USA [4]Huazhong Univ Sci & Technol, Tongji Med Coll, Tongji Hosp, Dept Otolaryngol, Wuhan 430074, Peoples R China [5]Ctr Postgrad Med Educ, Dept Biochem & Mol Biol, Warsaw, Poland
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关键词: Pendrin SLC26A4 periostin Muc5AC chronic rhinosinusitis nasal polyp mucus mucociliary clearance nasal epithelial cells

摘要:
Background: Chronic rhinosinusitis (CRS) is a multifactorial disease of unknown cause characterized by sinonasal inflammation, increased mucus production, and defective mucociliary clearance. Expression of Pendrin, an epithelial anion transporter, is increased in asthma and chronic obstructive pulmonary disease. Pendrin increases mucus production and regulates mucociliary clearance. Objectives: We sought to investigate the expression of pendrin and the mucus-related protein Muc5AC in sinonasal tissues of control subjects and patients with CRS and to evaluate the regulation of pendrin expression in nasal epithelial cells (NECs) in vitro. Methods: The expression and distribution of pendrin in sinonasal tissues was analyzed by using real-time PCR, immunoblot analysis, and immunohistochemistry. Differentiated NECs were used to study the regulation of pendrin expression. Results: Increased pendrin expression was observed in nasal polyp (NP) tissue of patients with CRS. Immunohistochemistry analysis revealed that pendrin was largely restricted to the epithelial layer. Pendrin expression significantly correlated with inflammatory cell markers, suggesting that the factors made by these cells might induce pendrin expression. Furthermore, both pendrin and periostin levels (a biomarker in asthma) correlated with IL-13 levels, suggesting that pendrin can be induced by this cytokine in sinonasal tissues. Expression of the mucus component protein Muc5AC correlated weakly with pendrin expression, indicating that pendrin might modulate mucus production in NPs. In cultured NECs pendrin expression was induced by T(H)2 cytokines and induced synergistically when TH2 cytokines were combined with IL-17A. Interestingly, human rhinovirus had a potentiating effect on IL-13-induced pendrin expression. Dexamethasone suppressed pendrin expression, suggesting that the therapeutic benefit of dexamethasone in asthmatic patients and those with CRS might involve regulation of pendrin expression. Conclusions: TH2-mediated pendrin expression is increased in NPs of patients with CRS and might lead to increased inflammation, mucus production, and decreased mucociliary clearance.

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出版当年[2014]版:
大类 | 1 区 医学
小类 | 1 区 过敏 1 区 免疫学
最新[2025]版:
大类 | 1 区 医学
小类 | 1 区 过敏 1 区 免疫学
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出版当年[2013]版:
Q1 ALLERGY Q1 IMMUNOLOGY
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Q1 ALLERGY Q1 IMMUNOLOGY

影响因子: 最新[2024版] 最新五年平均 出版当年[2013版] 出版当年五年平均 出版前一年[2012版] 出版后一年[2014版]

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第一作者单位: [1]Northwestern Univ, Div Allergy & Immunol, Feinberg Sch Med, Chicago, IL 60611 USA
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通讯机构: [1]Northwestern Univ, Div Allergy & Immunol, Feinberg Sch Med, Chicago, IL 60611 USA [2]Northwestern Univ, Dept Otolaryngol Head & Neck Surg, Feinberg Sch Med, Chicago, IL 60611 USA [*1]Northwestern Univ, Div Allergy & Immunol, Feinberg Sch Med, 240 E Huron St,McGaw Rm M-318, Chicago, IL 60611 USA
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