Tobacco Smoking Could Accentuate Epithelial-Mesenchymal Transition and Th2-Type Response in Patients With Chronic Rhinosinusitis With Nasal Polyps.

IF 4.3 4区 医学 Q2 IMMUNOLOGY
Immune Network Pub Date : 2022-06-15 eCollection Date: 2022-08-01 DOI:10.4110/in.2022.22.e35
Ki-Il Lee, Younghwan Han, Jae-Sung Ryu, Seung Min In, Jong-Yeup Kim, Joong Su Park, Jong-Seok Kim, Juhye Kim, Jubin Youn, Seok-Rae Park
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引用次数: 2

Abstract

Tobacco smoking (TS) has been known as one of the most potent risk factors for airway inflammatory diseases. However, there has been a paucity of information regarding the immunologic alteration mediated by TS in patients with chronic rhinosinusitis with nasal polyps (CRSwNP). To identify the effect of TS, we harvested human tissue samples (never smoker: n=41, current smoker: n=22, quitter: n=23) and analyzed the expression of epithelial-derived cytokines (EDCs) such as IL-25, IL-33, and thymic stromal lymphopoietin. The expressions of Th2 cytokines and total serum IgE showed a type-2 inflammatory alteration by TS. In addition, the epithelial marker E-cadherin and epithelial-mesenchymal transition (EMT)-associated markers (N-cadherin, α-SMA, and vimentin) were evaluated. Histological analysis showed that EDC expressions were upregulated in the current smoker group and downregulated in the quitter group. These expression patterns were consistent with mRNA and protein expression levels. We also found that the local Th2 cytokine expression and IgE class switching, as well as serum IgE levels, were elevated in the current smoker group and showed normal levels in the quitter group. Furthermore, the expressions of E-cadherin decreased while those of N-cadherin, α-SMA, and vimentin increased in the current smoker group compared those in the never smoker group. Taken together, these results indicate that TS contributes to the deterioration of pathogenesis by releasing local EDCs and Th2 cytokines, resulting in EMT in patients with CRSwNP. We verified that alterations of immunological response by TS in sinonasal epithelium can play a vital role in leading to CRSwNP.

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吸烟可增强慢性鼻窦炎合并鼻息肉患者的上皮-间质转化和th2型反应。
吸烟(TS)已被认为是气道炎症性疾病最有效的危险因素之一。然而,关于TS在慢性鼻窦炎伴鼻息肉(CRSwNP)患者中介导的免疫改变的信息缺乏。为了确定TS的影响,我们收集了人体组织样本(从不吸烟者:n=41,目前吸烟者:n=22,戒烟者:n=23),并分析了上皮源性细胞因子(EDCs)的表达,如IL-25, IL-33和胸腺基质淋巴生成素。Th2细胞因子和血清总IgE的表达呈2型炎性改变,上皮标志物E-cadherin和上皮-间质转化(EMT)相关标志物N-cadherin、α-SMA和vimentin的表达也被检测。组织学分析显示,当前吸烟组EDC表达上调,戒烟组EDC表达下调。这些表达模式与mRNA和蛋白表达水平一致。我们还发现,吸烟组局部Th2细胞因子表达和IgE类转换以及血清IgE水平升高,戒烟组正常。与不吸烟组相比,吸烟组E-cadherin表达降低,N-cadherin、α-SMA、vimentin表达升高。综上所述,这些结果表明,TS通过释放局部EDCs和Th2细胞因子,导致CRSwNP患者发生EMT,从而导致发病机制恶化。我们证实TS对鼻粘膜免疫反应的改变可能在导致CRSwNP中起重要作用。
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来源期刊
Immune Network
Immune Network Immunology and Microbiology-Immunology
CiteScore
2.90
自引率
3.30%
发文量
36
期刊介绍: Immune Network publishes novel findings in basic and clinical immunology and aims to provide a medium through which researchers in various fields of immunology can share and connect. The journal focuses on advances and insights into the regulation of the immune system and the immunological mechanisms of various diseases. Research that provides integrated insights into translational immunology is given preference for publication. All submissions are evaluated based on originality, quality, clarity, and brevity
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