本文關(guān)鍵詞：TIM-1、TIM-3在人慢性牙周炎牙齦組織中肥大細(xì)胞上表達(dá)的研究　出處：《暨南大學(xué)》2015年碩士論文　論文類型：學(xué)位論文

  更多相關(guān)文章： 慢性牙周炎 肥大細(xì)胞 脫顆粒 類胰蛋白酶 TIM-1 TIM-3

【摘要】：背景:牙周炎(periodontitis)是指累及牙周支持組織的局部炎癥性破壞性疾病。牙周炎已被醫(yī)學(xué)界定論為繼癌癥、心腦血管疾病之后,威脅人類身體健康的第三大殺手,是導(dǎo)致牙齒脫落的主要原因。牙周炎以菌斑為始動(dòng)因子,牙齦卟啉單胞菌(Porphyromonas gingivalis,Pg)、伴放線放線桿菌(Actinobacillus actinomycetemcomitans,Aa)以及福賽坦氏菌(Tannerella forsythensis,Tf)等革蘭氏陰性厭氧菌大量堆積在牙齦邊緣引起牙周組織的炎癥反應(yīng)。同時(shí),牙周致病菌釋放的脂多糖(lipopolysaccharide,LPS)、抗原和毒性因子等致病成分,激發(fā)宿主免疫反應(yīng)引起機(jī)體免疫損傷,導(dǎo)致局部炎癥細(xì)胞浸潤(rùn)并釋放多種細(xì)胞因子,進(jìn)一步造成宿主牙周組織的破壞及牙槽骨的吸收。多種免疫細(xì)胞及細(xì)胞因子參與牙周炎的免疫調(diào)節(jié),宿主的易感性及牙周致病菌之間的相互作用決定了牙周炎的發(fā)生及進(jìn)展。近年來(lái)認(rèn)為,肥大細(xì)胞(mast cells,MCs)除了作為超敏反應(yīng)的主要效應(yīng)細(xì)胞外,MCs作為調(diào)節(jié)和效應(yīng)性免疫細(xì)胞在適應(yīng)性免疫反應(yīng)的調(diào)節(jié)和固有免疫的建立中發(fā)揮重要作用,主要參與粘膜炎癥、機(jī)體防御和組織修復(fù)等。MCs被激活后,可通過(guò)脫顆粒釋放一系列介質(zhì),引起炎癥反應(yīng)或參與機(jī)體防御反應(yīng),發(fā)揮多種免疫功能。研究顯示,在正常牙齦組織及牙周炎牙齦組織中均檢測(cè)到MCs。研究表明,類胰蛋白酶(tryptase)陽(yáng)性MCs在人慢性牙周炎牙齦組織中表達(dá)最為豐富,并隨牙周炎的病變程度的增加而表達(dá)升高。T細(xì)胞免疫球蛋白粘蛋白(T cell immunoglobulin mucin domain,TIM)基因家族是T細(xì)胞表面的跨膜蛋白家族。TIM-1和TIM-3是TIM家族中的兩個(gè)重要成員,分別在分化成熟的Th2細(xì)胞和Th1細(xì)胞上表達(dá),參與Th細(xì)胞免疫反應(yīng)的調(diào)控。目前tryptase-TIM-1、TIM-3雙陽(yáng)性MCs在人慢性牙周炎上的表達(dá)及功能尚不清楚,有關(guān)牙周炎牙齦組織tryptase-TIM-1、TIM-3雙陽(yáng)性MCs在牙周炎的發(fā)生和發(fā)展中的免疫調(diào)控作用尚未見(jiàn)報(bào)道。目的:本研究通過(guò)采集臨床不同病變程度的牙周炎牙齦組織標(biāo)本,經(jīng)HE染色、甲苯胺藍(lán)染色、免疫組織化學(xué)染色及免疫熒光雙染色法,觀察不同病變程度的牙周炎牙齦標(biāo)本的炎癥程度、MCs表達(dá)及脫顆粒情況,tryptase-TIM-1、TIM-3雙陽(yáng)性MCs的表達(dá)情況。通過(guò)對(duì)牙周炎牙齦組織的炎癥程度等級(jí)評(píng)分、計(jì)算MCs平均陽(yáng)性細(xì)胞率及脫顆粒率、tryptase-TIM-1、TIM-3雙陽(yáng)性MCs表達(dá)的密度,探討tryptase-TIM-1、TIM-3雙陽(yáng)性MCs在牙周感染中的作用及其作用機(jī)制。研究結(jié)果將對(duì)后續(xù)以肥大細(xì)胞TIM-1、TIM-3為靶點(diǎn)的慢性牙周炎免疫防治提供理論基礎(chǔ)和實(shí)驗(yàn)依據(jù)。方法:按納入標(biāo)準(zhǔn),將80例自愿參與本研究的受試者按慢性牙周炎分類標(biāo)準(zhǔn)分為4組:1)正常對(duì)照組20例;2)輕度慢性牙周炎組20例;3)中度慢性牙周炎組20例;4)重度慢性牙周炎組20例。牙齦標(biāo)本置于10%中性福爾馬林固定液中浸泡48 h以上,制作頰舌向5μm厚的牙齦組織連續(xù)切片。HE染色,于光學(xué)顯微鏡下觀察各組牙齦組織的組織學(xué)變化;甲苯胺藍(lán)染色及免疫組織化學(xué)染色,于光學(xué)顯微鏡下觀察各組牙齦組織中MCs募集及脫顆粒情況,并計(jì)算MCs平均陽(yáng)性細(xì)胞率及脫顆粒率;免疫熒光雙染色,于熒光顯微鏡及共聚焦顯微鏡下觀察tryptase-TIM-1、TIM-3雙陽(yáng)性MCs在牙齦組織中的表達(dá),并計(jì)算tryptase-TIM-1、TIM-3雙陽(yáng)性MCs的密度(cells/mm2)。使用統(tǒng)計(jì)學(xué)軟件SPSS 13.0對(duì)數(shù)據(jù)進(jìn)行分析處理,采用Wilcoxon符號(hào)秩檢驗(yàn)、Kruskal-Wallis H檢驗(yàn)、Nemenyi法檢驗(yàn)、單因素方差分析(one-way ANOVA)和Pearson相關(guān)分析,P0.05時(shí)認(rèn)為差異有統(tǒng)計(jì)學(xué)意義。結(jié)果:1、組織學(xué)觀察結(jié)果結(jié)果顯示,4組牙齦組織切片炎癥程度評(píng)分有差別,牙齦組織的炎癥反應(yīng)程度與慢性牙周炎的病變程度趨勢(shì)一致:1)與正常對(duì)照組相比,各牙周炎組牙齦組織中的炎癥細(xì)胞浸潤(rùn)明顯增多,慢性牙周炎組炎癥評(píng)分明顯高于正常對(duì)照組(P0.01);2)中度慢性牙周炎組的炎癥程度評(píng)分明顯高于輕度慢性牙周炎組(P0.01);3)重度慢性牙周炎組的炎癥程度評(píng)分明顯高于輕度和中度牙周炎組(P0.01)。2、甲苯胺藍(lán)染色及免疫組織化學(xué)染色結(jié)果結(jié)果顯示,甲苯胺藍(lán)染色與免疫組織化學(xué)染色的陽(yáng)性細(xì)胞分布情況大致相同:1)與甲苯胺藍(lán)染色相比,免疫組織化學(xué)染色中MCs平均陽(yáng)性細(xì)胞率及脫顆粒率更高(P0.05),顯色及脫顆�，F(xiàn)象更明顯;2)慢性牙周炎組牙齦組織中MCs表達(dá)及脫顆粒現(xiàn)象比正常對(duì)照組明顯增多,MCs平均陽(yáng)性細(xì)胞率及脫顆粒率明顯高于正常對(duì)照組(P0.01);3)中度慢性牙周炎組的MCs平均陽(yáng)性細(xì)胞率及脫顆粒率明顯高于輕度慢性牙周炎組(P0.01);4)重度慢性牙周炎組的MCs平均陽(yáng)性細(xì)胞率及脫顆粒率明顯高于輕、中度慢性牙周炎組(P0.01)。3、免疫熒光雙染色結(jié)果1)慢性牙周炎組tryptase-TIM-1、TIM-3雙陽(yáng)性MCs的密度比正常對(duì)照組明顯升高(P0.01);2)中度慢性牙周炎組的tryptase-TIM-1、TIM-3雙陽(yáng)性MCs的密度顯著高于輕度慢性牙周炎組(P0.01);3)重度慢性牙周炎組的tryptase-TIM-1、TIM-3雙陽(yáng)性MCs的密度顯著高于輕、中度慢性牙周炎組(P0.01)。4、MCs平均陽(yáng)性細(xì)胞率和脫顆粒率、tryptase-TIM-1、TIM-3雙陽(yáng)性MCs與慢性牙周炎病變程度相關(guān)性分析結(jié)果經(jīng)Pearson相關(guān)分析,各組MCs平均陽(yáng)性細(xì)胞率和脫顆粒率、tryptase-TIM-1、TIM-3雙陽(yáng)性MCs密度均與慢性牙周炎的病變程度存在明顯的正相關(guān)關(guān)系。結(jié)論:1、慢性牙周炎牙齦組織中MCs平均陽(yáng)性細(xì)胞率和脫顆粒率隨慢性牙周炎的病變程度加重而增加。2、慢性牙周炎牙齦組織中tryptase-TIM-1、TIM-3雙陽(yáng)性MCs的密度隨慢性牙周炎的病變程度加重而增加。3、牙齦組織中MCs募集和脫顆�？赡軈⑴c牙周感染免疫反應(yīng)的病理過(guò)程,在牙周疾病的發(fā)病和進(jìn)程中發(fā)揮重要作用;肥大細(xì)胞TIM-1、TIM-3可能參與慢性牙周炎的炎癥反應(yīng),在慢性牙周炎的發(fā)病及疾病進(jìn)程中發(fā)揮關(guān)鍵作用。
[Abstract]:Background: periodontitis (periodontitis) is a devastating disease involving the periodontal support tissue local inflammation. Periodontitis has been inconclusive as medicine after cancer, cardiovascular diseases, threats to the third major killer of human health, is a major cause of tooth loss. The plaque is the initiating factor of periodontitis, Porphyromonas gingivalis (Porphyromonas gingivalis, Pg), Actinobacillus actinomycetemcomitans (Actinobacillus actinomycetemcomitans Aa) and Forseth Staw S (Tannerella forsythensis, Tf) bacteria such as gram negative anaerobic bacteria mass accumulation caused by periodontal tissue inflammation in the gingival margin. At the same time, periodontal bacteria release induced by lipopolysaccharide (lipopolysaccharide, LPS). Antigen and virulence factors of pathogenic components, stimulate the host immune response caused by immune injury, causing local infiltration of inflammatory cells and release cytokines, further made To destroy the host periodontal tissue and alveolar bone absorption. A variety of immune cells and immune cytokines involved in the regulation of periodontitis, host susceptibility and interaction between periodontal pathogens determines the incidence and progression of periodontitis. In recent years, mast cells (mast cells, MCs) in addition to the main effect as hypersensitivity the outside of the cell, MCs as regulatory and effector immune cells play an important role in the establishment and regulation of innate immunity in the adaptive immune response, mainly involved in mucosal inflammation, immune defense and tissue repair after.MCs is activated by degranulation to release a series of medium, cause inflammation or immune reaction in host defense. A variety of functions. The results show that in normal gingival tissue and periodontal tissues were detected in MCs. studies show that tryptase (tryptase) positive MCs in patients with chronic periodontitis The most abundant expression in gingival tissue, and increased with the severity of periodontitis and increased expression of.T cell immunoglobulin mucin (T cell immunoglobulin mucin domain, TIM T) gene family is a cell surface transmembrane protein family.TIM-1 and TIM-3 are two important members in the TIM family, were expressed in Th2 cells and the differentiation of Th1 cells, is involved in regulation of Th cell immune response. At tryptase-TIM-1, the expression and function of TIM-3 double positive MCs in human chronic periodontitis on is not clear, the periodontal tissues tryptase-TIM-1, immune regulation of TIM-3 double positive MCs in the occurrence and development of periodontitis has not been reported. Objective: this through the study of the collection of the clinical severity of periodontitis gingival tissue specimens by HE staining, toluidine blue staining, immunohistochemical staining and double immunofluorescence staining, observe The degree of inflammation with the severity of periodontitis gingival tissues, the expression of MCs and degranulation, tryptase-TIM-1, expression of TIM-3 double positive MCs. The periodontal tissue inflammation score, MCs calculated the average rate of positive cells and degranulation rate, tryptase-TIM-1 expression, TIM-3 double positive MCs density of tryptase-TIM-1, TIM-3 double positive MCs in periodontal infection of the role and its mechanism. The results of the follow-up to the mast cell TIM-1, TIM-3 provide a theoretical basis and experimental basis for targeted immune prevention of chronic periodontitis. Methods: according to the inclusion criteria, subjects 80 volunteers participated in this study according to the classification standard of chronic periodontitis 4 group: 1) and 20 cases of normal control group; 2) mild chronic periodontitis group 20 cases; 3) moderate chronic periodontitis group 20 cases); 4 patients with severe chronic periodontitis and 20 cases of gingival specimens were placed in 10% neutral Holmes. Ma Lin fixed buffer for 48 h or more, making the buccolingual 5 m thick continuous gingival tissue slices were stained with.HE, were observed by microscope and the histological changes of gingival tissue in each group; toluidine blue staining and immunohistochemical staining were observed under optical microscope in gingival tissue of MCs recruitment and degranulation, and calculate the average MCs positive cell rate and degranulation rate; double immunofluorescent staining, fluorescent microscopy and confocal microscope tryptase-TIM-1, TIM-3 double positive expression of MCs in gingival tissue, and calculate the tryptase-TIM-1, TIM-3 double positive MCs density (cells/mm2). 13 on the use of statistical software SPSS data analysis and processing, using Wilcoxon signed rank test, Kruskal-Wallis H test, Nemenyi test, single factor analysis of variance (one-way ANOVA) and Pearson correlation analysis, P0.05 believes that there are significant differences. Results: 1. Histological observation results showed that 4 groups of gingival tissue slices inflammation score difference, consistent lesions trend degree of inflammatory reaction of gingival tissue with chronic periodontitis: 1) compared with the normal control group, the inflammatory cell infiltration in periodontitis gingival tissue increased significantly, chronic periodontitis group inflammation score significantly higher than the normal control group (P0.01); 2) moderate chronic periodontitis group the inflammation score was significantly higher than that of mild chronic periodontitis group (P0.01); 3) severe chronic periodontitis group inflammation score was significantly higher than that of mild and moderate periodontitis group (P0.01).2, toluidine blue staining and immunohistochemical staining showed that toluidine blue staining immunohistochemical staining positive cells and the distribution of roughly the same: 1) compared with toluidine blue staining, immunohistochemical staining of MCs positive cells and the average rate of The degranulation rate is higher (P0.05), color and degranulation phenomenon is more obvious; 2) and degranulation of the expression of MCs in gingival tissue of chronic periodontitis group was significantly increased than the normal control group and normal control group, the rate of degranulation was significantly higher than the average MCs positive cells (P0.01); 3) the average rate of MCs positive cells moderate chronic periodontitis group and degranulation rate was significantly higher than that of mild chronic periodontitis group (P0.01); 4) severe chronic periodontitis group MCs average rate of positive cells and degranulation rate was significantly higher than that of mild, moderate chronic periodontitis group (P0.01.3), double immunofluorescence staining results in 1 chronic periodontitis group) tryptase-TIM-1, TIM-3 double positive MCs the density was significantly higher than the normal control group (P0.01); 2) moderate chronic periodontitis group tryptase-TIM-1, TIM-3 double positive MCs density was significantly higher than that of mild chronic periodontitis group (P0.01); 3) severe chronic periodontitis group tryptase-TIM-1, TIM-3 The positive MCs density was significantly higher than that of light, moderate chronic periodontitis group (P0.01.4 MCs), the average rate of positive cells and degranulation rate, tryptase-TIM-1, MCs and TIM-3 double positive chronic periodontitis lesions correlation analysis results by Pearson correlation analysis, MCs was the average rate of positive cells and degranulation rate, tryptase-TIM-1, there is a significant positive correlation the lesions were chronic periodontitis and TIM-3 double positive MCs density. Conclusion: 1. The gingival tissues of patients with chronic periodontitis MCs average positive cell rate and degranulation rate with the severity of chronic periodontitis aggravates the increase of.2, tryptase-TIM-1 in gingival tissues of patients with chronic periodontitis and chronic periodontitis lesions with TIM-3 double positive MCs density increased the increase of.3, MCs in gingival tissue recruitment and degranulation of periodontal infection may be involved in the immune response of the pathological process in the pathogenesis of periodontal disease and in the course of play The mast cell TIM-1, TIM-3 may participate in the inflammatory response of chronic periodontitis, and play a key role in the pathogenesis of chronic periodontitis and the process of disease.

【學(xué)位授予單位】：暨南大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2015
【分類號(hào)】：R781.4

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