SOCS3及Eotaxin-2在变应性鼻炎中的表达及意义

发布时间：2018-04-13 22:38

本文选题：鼻炎 + 变应性　；参考：《山东大学》2010年硕士论文

【摘要】： 背景：变应性鼻炎是Th2细胞及其细胞因子占优势的变态反应。Th2细胞主要合成和分泌IL-4、IL-5、IL-6、IL-10、IL-13等细胞因子。SOCS(suppressor of cytokine singnaling,细胞因子信号转导抑制因子)是近年来新发现的一类负向调节蛋白,可抑制多种细胞因子的信号通路,且大多数成员可被细胞因子和生长因子所诱导产生。其中SOCS3在Th2细胞中的表达是Th1细胞的23倍。IL-4等细胞因子能诱导SOCS3在Th2细胞上的表达,而SOCS3蛋白通过对IL-12/STAT4等通路的抑制可抑制Th1细胞及其细胞因子的产生。嗜酸性粒细胞增多是变应性鼻炎主要病理表现之一,Eotaxin-2为嗜酸性粒细胞趋化因子之一。Eotaxin-2(CCL24)与Eotaxin-1(CCL11) Eotaxin-3(CCL26)同属于趋化因子CC亚家族成员,他们均选择性的专一的与其共同的受体CCR3结合进而趋化并激活嗜酸性粒细胞。三种趋化因子的生物学作用相似,与嗜酸性粒细胞表面的受体CCR3结合后可促使嗜酸性粒细胞合成LTC4、产生活性氧簇、脱颗粒释放炎性介质等从而发挥其效应器功能。研究发现在鼻息肉患者和哮喘患者中,IL-4、IL-13等细胞因子能诱导鼻黏膜和支气管黏膜单核细胞、上皮细胞等表达Eotaxin-2增多,其中IL-4诱导鼻黏膜和支气管黏膜表达Eotaxin-2能力较强。目的：本实验通过应用免疫组化技术研究SOCS3及Eotaxin-2在变态反应性鼻炎鼻粘膜中的表达,通过二者相关性,分析SOCS3对Eotaxin-2的影响,进一步探讨SOCS3在变态反应性鼻炎发病机制中的作用及对临床症状的影响。方法：按照2004年兰州会议关于变态反应性鼻炎的诊断标准,选取20例AR患者鼻粘膜为实验组和15例单纯鼻中隔偏曲患者鼻粘膜为对照组,应用免疫组织化学技术分别检测SOCS3及Eotaxin-2的表达,结果以(x±s)表示,组间差异性比较用t检验,并用直线相关分析法对SOCS3及Eotaxin-2表达的相关性进行分析。结果：在AR患者鼻黏膜中,SOCS3及Eotaxin-2的表达上调,在鼻黏膜炎性细胞、上皮细胞、腺体细胞、血管内皮细胞呈显著性表达。平均光密度值SOCS3为0.2401±0.01463, Eotaxin-2为0.2398±0.01423,与对照组相比,均P0.01,差异有统计学意义。AR患者鼻黏膜中SOCS3及Eotaxin-2的表达具相关性(r=0.951,P0.01)。结论：AR患者SOCS3及Eotaxin-2在鼻黏膜组织中表达增高,且二者呈正相关。此结果可能由于SOCS3增强Th2细胞反应,间接导致Eotaxin-2增多。也可能是SOCS3与Eotaxin-2直接相互诱导所致。确切机制有待进一步研究。
[Abstract]:Background : Allergic rhinitis is a Th2 cell and its cytokine - dominated allergy . Th2 cells mainly synthesize and secrete cytokines such as IL - 4 , IL - 5 , IL - 6 , IL - 10 , IL - 13 , etc . SOCS ( cytokine of cytokine singnaling , cytokine signal transduction inhibitory factor ) is a kind of negative regulatory protein which has been newly discovered in recent years . SOCS ( cytokine of cytokine singnaling , cytokine signal transduction inhibitory factor ) is 23 times that of Th1 cells .

Eotaxin - 2 is one of the main pathological manifestations of allergic rhinitis . Eotaxin - 2 is one of eotaxin . Eotaxin - 2 ( CCL 24 ) and Eotaxin - 1 ( CCL 11 ) Eotaxin - 3 ( CCL 26 ) bind to chemokine CC sub - family members . They both selectively bind to their common receptor CCR3 and activate eosinophils . Three kinds of chemokine have similar biological effects , which can induce eosinophils to synthesize LTC4 , produce reactive oxygen clusters , release inflammatory mediators , and so on , so as to exert their effector functions .

It was found that IL - 4 , IL - 13 and other cytokines could induce the expression of Eotaxin - 2 in nasal mucosa and bronchial mucosa mononuclear cells and epithelial cells in patients with nasal polyps and asthma , and IL - 4 induced the expression of Eotaxin - 2 in nasal mucosa and bronchial mucosa .

Objective : To study the effects of SOC3 and Eotaxin - 2 on Eotaxin - 2 in the nasal mucosa of allergic rhinitis by using immunohistochemistry . The effect of SO3 on Eotaxin - 2 and its effect on the pathogenesis of allergic rhinitis were discussed .

Methods : According to the criteria for diagnosis of allergic rhinitis in Lanzhou Conference in 2004 , the nasal mucosa of 20 patients with AR was selected as experimental group and 15 patients with simple nasal septum deviation . The results were as follows : ( x 卤 s ) , the difference between groups was examined by t , and the correlation between SO3 and Eotaxin - 2 expression was analyzed by linear correlation analysis .

Results : In the nasal mucosa of AR patients , the expression of SOC3 and Eotaxin - 2 was up - regulated . The mean optical density value SOC3 was 0.2398 卤 0.01463 , Eotaxin - 2 was 0.2398 卤 0.01423 , and the expression of Eotaxin - 2 was correlated with the control group ( r = 0.951 , P0.01 ) .

Conclusion : The expression of SO 3 and Eotaxin - 2 in the nasal mucosa of AR patients is higher than that of Eotaxin - 2 , which may also be caused by the direct mutual induction of SO3 and Eotaxin - 2 . The exact mechanism is to be further studied .

【学位授予单位】：山东大学
【学位级别】：硕士
【学位授予年份】：2010
【分类号】：R765.21

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