本文選題：結(jié)核 + 病理　； 參考：《蘭州大學(xué)》2009年碩士論文

【摘要】： 第一部分:分枝桿菌所致家兔皮膚液化病理模型研究 研究目的皮內(nèi)接種免疫建立BCG、H37Ra和恥垢分枝桿菌感染的新西蘭兔皮膚模型,為肺結(jié)核干酪樣壞死和繼而發(fā)生的液化提供研究模型。 材料和方法將三種菌株卡介苗(Bacillus Calmette-Guerin,BCG),恥垢分枝桿菌(M.smegmatis),H37Ra株配置成5×106CFU、5×104CFU、5×102CFU菌液。對(duì)健康新西蘭兔初次免疫分別行皮內(nèi)注射5×106CFU、5×104CFU、5×102CFU的BCG、H37Ra和恥垢分枝桿菌菌液。6周后在病灶周圍再次以相同劑量行皮內(nèi)注射進(jìn)行加強(qiáng)免疫,加強(qiáng)免疫后14天后病變明顯時(shí)取材,以石蠟包埋,制作切片并行HE染色于鏡下觀察。 結(jié)果新西蘭兔分別經(jīng)皮內(nèi)接種BCG、H37Ra和恥垢分枝桿菌后,高劑量組觀察到明顯的炎癥反應(yīng)和膿腫液化、破潰等病理改變。再次免疫后可觀察到Koch現(xiàn)象。引起病變的嚴(yán)重程度依次為BCG強(qiáng)于H37Ra,后者又強(qiáng)于恥垢分枝桿菌。皮膚模型處取材行細(xì)菌抗酸染色,結(jié)果呈陽(yáng)性。三組病灶切片的顯微病理改變均可觀察到典型的結(jié)核結(jié)節(jié)樣病灶。BCG中、低劑量組再次免疫后可誘導(dǎo)產(chǎn)生小結(jié)節(jié)樣改變,但不發(fā)生液化潰瘍,H37Ra中劑量組和恥垢分枝桿菌中劑量組及所有低劑量組均沒(méi)有觀察到明顯的病理改變。 結(jié)論分枝桿菌引起的皮膚干酪樣壞死和液化與感染細(xì)菌劑量密切相關(guān),5X106CFU/ml濃度的分枝桿菌可有效誘導(dǎo)新西蘭兔皮膚病灶發(fā)生液化和壞死,其中BCG引起的病理改變最明顯。 第二部分:人空洞型肺結(jié)核病理組織CD4、CD8、CD25和CD68分子表達(dá)分析 研究目的應(yīng)用免疫組織化學(xué)技術(shù)檢測(cè)慢性纖維空洞型肺結(jié)核病人肺病理組織中CD4~+T、CD8~+T、CD25~+T淋巴細(xì)胞和CD68~+巨噬細(xì)胞的增殖情況及分布特點(diǎn),探究肺結(jié)核發(fā)生發(fā)展的免疫機(jī)制。 材料和方法蘭州市肺科醫(yī)院2005至2006年肺結(jié)核病人手術(shù)標(biāo)本中選取的10例石蠟標(biāo)本。應(yīng)用免疫組織化學(xué)兩步法檢測(cè)10例空洞性肺結(jié)核干酪樣壞死組織石蠟切片中CD4、CD8、CD25和CD68陽(yáng)性細(xì)胞分布特征。 結(jié)果在空洞性結(jié)核為主的結(jié)核組織中,以壞死部位為中心,各種免疫細(xì)胞出現(xiàn)了明顯的分層分布和在壞死外周出現(xiàn)了大量的細(xì)胞浸潤(rùn)。在外周細(xì)胞浸潤(rùn)細(xì)胞中,CD25+T淋巴細(xì)胞為中心CD4~+ T和CDS~+ T細(xì)胞聚集,CD68+巨噬細(xì)胞也少量聚集。 結(jié)論外周細(xì)胞浸潤(rùn)處以CD25+ T淋巴細(xì)胞為中心的細(xì)胞浸潤(rùn)區(qū)域是宿主病原菌相互作用的免疫活性中心。
[Abstract]:Part one: study on the pathological model of skin liquefaction induced by mycobacterium in rabbits objective to establish the skin model of New Zealand rabbits infected by BCGH37Ra and Mycobacterium smeareus by intradermal immunization. To provide a research model for caseous necrosis and subsequent liquefaction of pulmonary tuberculosis. Materials and methods three strains of Bacillus Calmette-Guerinen BCG and M.smegmatis H37Ra strain were divided into 5 脳 10 6 CFU 5 脳 10 4 CFU 5 脳 10 2 CFU solution. Healthy New Zealand rabbits were immunized by intradermal injection of 5 脳 10 6 CFU 5 脳 10 4 CFU 5 脳 10 2 CFU 5 脳 10 2 CFU respectively. After 6 weeks, the rabbits were immunized again with the same dose of intradermal injection around the lesion. Paraffin embedded sections were made and stained with HE under microscope. Results after intradermal inoculation of BCGH37Ra and Mycobacterium smegmatis in New Zealand rabbits, obvious inflammatory reaction, liquefaction and rupture of abscess were observed in high dose group. Koch phenomenon was observed after reimmunization. The severity of BCG was stronger than that of H37 Ra.The latter was stronger than Mycobacterium smearus. Bacterial acid-fast staining was performed on the skin model and the results were positive. In the typical tuberculous nodular lesion. BCG was observed in the micropathological changes of the lesion sections in the three groups. The small nodular changes could be induced in the low dose group after repeated immunization. However, no significant pathological changes were observed in the medium dose group of H37Ra, the medium dose group of Mycobacterium smearus and all the low dose groups. Conclusion the keratinoid necrosis and liquefaction caused by mycobacterium can induce liquefaction and necrosis of skin lesions in New Zealand rabbits with the concentration of 5X106 CFU / ml. The pathological changes caused by BCG are the most obvious. The second part: expression of CD4, CD8, CD25 and CD68 in human cavitary pulmonary tuberculosis objective to detect the expression of CD4 ~ T ~ + CD8 ~ in lung tissues of patients with chronic fibrous cavitation pulmonary tuberculosis by immunohistochemical technique The proliferation and distribution of CD25 ~ T lymphocytes and CD68 ~ macrophages. To explore the immune mechanism for the occurrence and development of pulmonary tuberculosis. Materials and methods Ten paraffin specimens from pulmonary tuberculosis patients from 2005 to 2006 were selected. Immunohistochemical two-step method was used to detect the distribution of CD4 + CD8 + CD25 and CD68 positive cells in paraffin sections of 10 caseous necrotic tissues of pulmonary tuberculosis. Results in the tuberculous tissues with cavitary tuberculosis, the necrotic site was the center, and the various immune cells were obviously stratified and infiltrated in the necrotic periphery. In peripheral infiltrating cells, CD25 T lymphocytes were the center of CD4T and CDS- T cells, and CD68 macrophages were also concentrated in a small amount. Conclusion the infiltrating area of peripheral cells with CD25 T lymphocytes as the center is the immune active center of host pathogen interaction.
【學(xué)位授予單位】：蘭州大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2009
【分類號(hào)】：R52;R392

【引證文獻(xiàn)】

相關(guān)碩士學(xué)位論文 前1條

1 魏晶;高通量測(cè)序技術(shù)分析肺結(jié)核患者和潛伏感染者PBMC基因表達(dá)譜差異[D];華南理工大學(xué);2013年

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本文編號(hào)：2096275