發(fā)布時(shí)間：2018-05-15 09:39

  本文選題：肺炎支原體 + 特發(fā)性血小板減少性紫癜　； 參考：《蚌埠醫(yī)學(xué)院》2012年碩士論文

【摘要】：目的：本實(shí)驗(yàn)旨在通過(guò)建立BALB/C小鼠肺炎支原體感染肺外器官損害模型，研究小鼠肺炎支原體感染致血小板減少性紫癜與細(xì)胞免疫的相關(guān)性，探討細(xì)胞免疫sIL-2R、CD_4~+、CD_8~+、CD_4~+/CD_8~+在肺炎支原體感染致血小板減少性紫癜中的作用，從而進(jìn)一步闡述肺炎支原體感染后引發(fā)血小板減少性紫癜的發(fā)病機(jī)制。 方法：將8周齡的BALB/C小鼠80只隨機(jī)分成兩組，實(shí)驗(yàn)組48只，對(duì)照組32只。在0、1、2三天，實(shí)驗(yàn)組經(jīng)鼻接種肺炎支原體菌液三次；對(duì)照組經(jīng)鼻滴入等量肺炎支原體培養(yǎng)基。接種后觀察小鼠的活動(dòng)情況、飲食情況、體型、毛發(fā)、呼吸道分泌物及呼吸情況等。分別在第4、8、12、16、20、24、28、32天處死。摘眼球取血，分別行血小板計(jì)數(shù)、用ELISA檢測(cè)sIL-2R、用流式細(xì)胞儀測(cè)T細(xì)胞亞群CD_4~+、CD_8~+、CD_4~+/CD_8~+，所有肺組織作病理切片，并作肺組織病理評(píng)分來(lái)確定小鼠肺組織的炎癥反應(yīng)程度。取肺組織作勻漿培養(yǎng)作病原學(xué)檢測(cè)。 結(jié)果：接種動(dòng)物全部存活無(wú)死亡，實(shí)驗(yàn)組動(dòng)物肺部病理切片均顯示不同程度的肺炎支原體肺炎病理?yè)p害表現(xiàn)，病理學(xué)評(píng)分在1.87～12.68之間，對(duì)照組肺組織病理切片無(wú)明顯病理?yè)p害表現(xiàn)。試驗(yàn)組的細(xì)胞因子sIL-2R、CD_8~+明顯比對(duì)照組升高，CD_4~+、CD_4~+/CD_8~+比對(duì)照組低，試驗(yàn)組血小板的均數(shù)明顯低于對(duì)照組且有統(tǒng)計(jì)學(xué)意義。 結(jié)論：成功建立BALB/c小鼠肺炎支原體感染模型；肺炎支原體感染可導(dǎo)致肺外器官損害，細(xì)胞免疫在肺炎支原體感染致血小板減少性紫癜中起了重要的作用，且sIL-2R水平的高低直接反應(yīng)了病情的輕重。
[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.
【學(xué)位授予單位】：蚌埠醫(yī)學(xué)院
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2012
【分類號(hào)】：R725.6

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本文編號(hào)：1891918