C型凝集素DC-SIGN在人牙髓组织中表达的免疫组化研究
发布时间：2018-10-19 08:52
【摘要】：细菌感染是牙髓炎的主要病因,常由于各种原因的牙体硬组织破坏,细菌入侵牙髓而诱发感染。G-菌是牙髓炎的主要致病菌,胞壁中的LPS是其主要毒力因子,同宿主其他部位一样,牙髓炎症是宿主对病原体的免疫反应,牙髓组织破坏和修复之间的关系决定了牙髓组织的活力及其炎症程度。在宿主免疫反应中,免疫细胞及非免疫细胞能够表达模式识别受体(PPR)来识别并结合病原体,进而诱导炎症反应。DC-SIGN是模式识别受体C型凝集素中的成员,它既能激活初始免疫应答,又能抑制免疫反应,具有正负免疫调节作用,是近年来研究的热点。DC-SIGN主要分布在树突状细胞和巨噬细胞中,兼具细胞黏附受体和模式识别受体功能,在特异性及非特异性免疫反应中都发挥作用。目前关于DC-SIGN在人炎性牙髓组织中的作用未见报道,其在牙髓疾病中的发生、发展的作用机理也尚不清楚。本实验应用免疫组织化学检测法初步探讨DC-SIGN在人牙髓炎症过程中的表达及作用。实验目的:应用免疫组织化学的方法,观察DC-SIGN在正常及急、慢性人牙髓组织中的表达和定位情况,并对其结果进行统计学分析,初步探讨DC-SIGN在人牙髓炎中的作用机制。实验方法:收集于吉林大学口腔医院就诊患者的新鲜牙髓组织,经固定、包埋、切片、HE染色,应用光学显微镜观察牙髓组织病理学变化,并结合患者的临床表现,作为牙髓组织分组依据,将组织标本分为三组。其中,正常牙髓组镜下表现为成纤维细胞、未分化间充质细胞、毛细血管及胶原纤维;急性炎症牙髓组镜下表现为血管扩张充血,中性粒细胞广泛浸润,局部组织液化坏死;慢性炎症牙髓组镜下表现为血管扩张充血,组织水肿,淋巴细胞、浆细胞、巨噬细胞、中性粒细胞等慢性炎症细胞浸润。免疫组织化学方法观察DC-SIGN在三组标本中的定位和表达情况。使用显微照相系统和Image-pro-plus图像分析软件对各组DC-SIGN阳性部位进行平均光密度测定,进行统计学处理,评价三组牙髓组织中DC-SIGN的定位和表达情况。结果:HE染色观察到急慢性炎症牙髓组中血管扩张充血,炎性细胞广泛浸润。免疫组织化学法观察到,三组牙髓组织中均有DC-SIGN表达,但不同组别其平均光密度值不同,DC-SIGN在正常牙髓组织中表达少,在炎症性牙髓组织中表达增多。结论:DC-SIGN在人炎症性牙髓组织中有表达,并参与牙髓炎的发生、发展过程。
[Abstract]:Bacterial infection is the main cause of pulpitis, which is often induced by the destruction of hard tissue of dental body and the invasion of dental pulp by bacteria. G- bacteria is the main pathogen of pulpitis, and LPS in the cell wall is the main virulence factor. Just like other parts of the host, dental pulp inflammation is the host's immune response to pathogens. The relationship between the destruction and repair of dental pulp tissue determines the activity of dental pulp tissue and the degree of inflammation. In the host immune response, immune cells and non-immune cells can express pattern recognition receptor (PPR) to recognize and bind pathogens, and then induce inflammatory response. DC-SIGN is a member of pattern recognition receptor C lectin. It not only activates the initial immune response, but also inhibits the immune response. It has both positive and negative immunomodulatory effects, and is a hot topic in recent years. DC-SIGN mainly distributes in dendritic cells and macrophages, and has the functions of cell adhesion receptor and pattern recognition receptor. Play a role in both specific and nonspecific immune responses. At present, the role of DC-SIGN in human inflammatory dental pulp tissue has not been reported, and the mechanism of its occurrence and development in dental pulp disease is still unclear. The expression and role of DC-SIGN in human dental pulp inflammation were studied by immunohistochemical method. Objective: to observe the expression and localization of DC-SIGN in normal, acute and chronic human dental pulp by immunohistochemical method, and to analyze the results statistically, and to explore the mechanism of DC-SIGN in human pulpitis. Methods: the fresh dental pulp tissue was collected from the patients in Jilin University Stomatology Hospital. The pathological changes of dental pulp were observed by optical microscope after fixation, embedding, sectioning, HE staining, and combined with the clinical manifestations of the patients. As the basis of pulp tissue grouping, tissue specimens were divided into three groups. Among them, fibroblasts, undifferentiated mesenchymal cells, capillaries and collagen fibers were observed under microscope in the normal dental pulp group, and vasodontic hyperemia, extensive infiltration of neutrophils and local tissue liquefaction and necrosis were observed in the acute inflammatory dental pulp group. The chronic inflammatory pulp group showed vasodontic hyperemia, tissue edema, infiltration of lymphocytes, plasma cells, macrophages, neutrophils and other chronic inflammatory cells. Immunohistochemical method was used to observe the localization and expression of DC-SIGN in the three groups. The mean optical density of the positive parts of DC-SIGN in each group was measured by microphotography system and Image-pro-plus image analysis software. The location and expression of DC-SIGN in three groups of dental pulp tissues were evaluated by statistical analysis. Results: vascular dilation and hyperemia and extensive infiltration of inflammatory cells were observed in acute and chronic inflammatory pulp group by HE staining. The expression of DC-SIGN was observed by immunohistochemical method in the three groups, but the average optical density was different in different groups. The expression of DC-SIGN was less in the normal dental pulp tissue and increased in the inflammatory pulp tissue. Conclusion: DC-SIGN is expressed in human inflammatory pulp tissue and is involved in the occurrence and development of pulpitis.
【学位授予单位】：吉林大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R781
[Abstract]:Bacterial infection is the main cause of pulpitis, which is often induced by the destruction of hard tissue of dental body and the invasion of dental pulp by bacteria. G- bacteria is the main pathogen of pulpitis, and LPS in the cell wall is the main virulence factor. Just like other parts of the host, dental pulp inflammation is the host's immune response to pathogens. The relationship between the destruction and repair of dental pulp tissue determines the activity of dental pulp tissue and the degree of inflammation. In the host immune response, immune cells and non-immune cells can express pattern recognition receptor (PPR) to recognize and bind pathogens, and then induce inflammatory response. DC-SIGN is a member of pattern recognition receptor C lectin. It not only activates the initial immune response, but also inhibits the immune response. It has both positive and negative immunomodulatory effects, and is a hot topic in recent years. DC-SIGN mainly distributes in dendritic cells and macrophages, and has the functions of cell adhesion receptor and pattern recognition receptor. Play a role in both specific and nonspecific immune responses. At present, the role of DC-SIGN in human inflammatory dental pulp tissue has not been reported, and the mechanism of its occurrence and development in dental pulp disease is still unclear. The expression and role of DC-SIGN in human dental pulp inflammation were studied by immunohistochemical method. Objective: to observe the expression and localization of DC-SIGN in normal, acute and chronic human dental pulp by immunohistochemical method, and to analyze the results statistically, and to explore the mechanism of DC-SIGN in human pulpitis. Methods: the fresh dental pulp tissue was collected from the patients in Jilin University Stomatology Hospital. The pathological changes of dental pulp were observed by optical microscope after fixation, embedding, sectioning, HE staining, and combined with the clinical manifestations of the patients. As the basis of pulp tissue grouping, tissue specimens were divided into three groups. Among them, fibroblasts, undifferentiated mesenchymal cells, capillaries and collagen fibers were observed under microscope in the normal dental pulp group, and vasodontic hyperemia, extensive infiltration of neutrophils and local tissue liquefaction and necrosis were observed in the acute inflammatory dental pulp group. The chronic inflammatory pulp group showed vasodontic hyperemia, tissue edema, infiltration of lymphocytes, plasma cells, macrophages, neutrophils and other chronic inflammatory cells. Immunohistochemical method was used to observe the localization and expression of DC-SIGN in the three groups. The mean optical density of the positive parts of DC-SIGN in each group was measured by microphotography system and Image-pro-plus image analysis software. The location and expression of DC-SIGN in three groups of dental pulp tissues were evaluated by statistical analysis. Results: vascular dilation and hyperemia and extensive infiltration of inflammatory cells were observed in acute and chronic inflammatory pulp group by HE staining. The expression of DC-SIGN was observed by immunohistochemical method in the three groups, but the average optical density was different in different groups. The expression of DC-SIGN was less in the normal dental pulp tissue and increased in the inflammatory pulp tissue. Conclusion: DC-SIGN is expressed in human inflammatory pulp tissue and is involved in the occurrence and development of pulpitis.
【学位授予单位】：吉林大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R781
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