细胞免疫在肺炎支原体感染致血小板减少性紫癜发病机制的研究

发布时间：2018-05-15 09:39

本文选题：肺炎支原体 + 特发性血小板减少性紫癜　；参考：《蚌埠医学院》2012年硕士论文

【摘要】：目的：本实验旨在通过建立BALB/C小鼠肺炎支原体感染肺外器官损害模型，研究小鼠肺炎支原体感染致血小板减少性紫癜与细胞免疫的相关性，探讨细胞免疫sIL-2R、CD_4~+、CD_8~+、CD_4~+/CD_8~+在肺炎支原体感染致血小板减少性紫癜中的作用，从而进一步阐述肺炎支原体感染后引发血小板减少性紫癜的发病机制。方法：将8周龄的BALB/C小鼠80只随机分成两组，实验组48只，对照组32只。在0、1、2三天，实验组经鼻接种肺炎支原体菌液三次；对照组经鼻滴入等量肺炎支原体培养基。接种后观察小鼠的活动情况、饮食情况、体型、毛发、呼吸道分泌物及呼吸情况等。分别在第4、8、12、16、20、24、28、32天处死。摘眼球取血，分别行血小板计数、用ELISA检测sIL-2R、用流式细胞仪测T细胞亚群CD_4~+、CD_8~+、CD_4~+/CD_8~+，所有肺组织作病理切片，并作肺组织病理评分来确定小鼠肺组织的炎症反应程度。取肺组织作匀浆培养作病原学检测。结果：接种动物全部存活无死亡，实验组动物肺部病理切片均显示不同程度的肺炎支原体肺炎病理损害表现，病理学评分在1.87～12.68之间，对照组肺组织病理切片无明显病理损害表现。试验组的细胞因子sIL-2R、CD_8~+明显比对照组升高，CD_4~+、CD_4~+/CD_8~+比对照组低，试验组血小板的均数明显低于对照组且有统计学意义。结论：成功建立BALB/c小鼠肺炎支原体感染模型；肺炎支原体感染可导致肺外器官损害，细胞免疫在肺炎支原体感染致血小板减少性紫癜中起了重要的作用，且sIL-2R水平的高低直接反应了病情的轻重。
[Abstract]:Objective: to study the relationship between Thrombocytopenic purpura and cellular immunity in BALB/C mice by establishing the model of pulmonary organ damage caused by mycoplasma pneumoniae infection. Objective: to investigate the role of cellular immunity of sIL-2R + CD4 ~ + CD8 / CD8 in the pathogenesis of thrombocytopenic purpura caused by mycoplasma pneumoniae infection, so as to further elucidate the pathogenesis of thrombocytopenic purpura caused by mycoplasma pneumoniae infection. Methods: 80 BALB/C mice aged 8 weeks were randomly divided into two groups: experimental group (n = 48) and control group (n = 32). After 23 days, the experimental group was inoculated with mycoplasma pneumoniae solution three times, and the control group was infused with the same amount of mycoplasma pneumoniae medium. After inoculation, the activity, diet, body size, hair, respiratory secretion and respiration of mice were observed. They were executed for 32 days on the 4th hour, the 8th hour, the 12th hour, the 16th hour, the 20th hour, the other 28 days. Blood was taken from eyeball, platelet count was performed separately, sIL-2R was detected by ELISA, CD4 ~ + CD8 ~ / CD8 ~ in T cell subgroup was measured by flow cytometry, all lung tissues were made pathological section and lung tissue pathological score was used to determine the degree of inflammatory reaction in mouse lung tissue. Lung tissue was taken as homogenate culture for etiological detection. Results: all of the inoculated animals survived without death. The lung pathological sections of the experimental group showed different degrees of pathological damage of mycoplasma pneumoniae pneumonia, and the pathological score was between 1.87 and 12.68. There was no obvious pathological damage in the control group. Compared with the control group, the cytokines of the experimental group were significantly higher than that of the control group. The mean number of platelet in the experimental group was significantly lower than that in the control group, and the mean number of the platelets in the experimental group was significantly lower than that in the control group. Conclusion: the BALB/c mouse model of mycoplasma pneumoniae infection can be successfully established, and mycoplasma pneumoniae infection can cause damage to the extrapulmonary organs, and cellular immunity plays an important role in the pathogenesis of thrombocytopenic purpura caused by mycoplasma pneumoniae infection. And the level of sIL-2R directly reflects the severity of the disease.
【学位授予单位】：蚌埠医学院
【学位级别】：硕士
【学位授予年份】：2012
【分类号】：R725.6

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