發(fā)布時(shí)間：2018-04-19 20:38

  本文選題：結(jié)核病 + 空洞型肺結(jié)核　； 參考：《蘭州大學(xué)》2017年碩士論文

【摘要】：全世界范圍內(nèi),結(jié)核病的感染率和致死率都非常高,尤其是在中國和印度等發(fā)展中國家,結(jié)核病給社會(huì)以及個(gè)人帶來了沉重的負(fù)擔(dān)。在結(jié)核分枝桿菌感染的初期,大多數(shù)人能通過自身免疫力阻止結(jié)核病的進(jìn)一步發(fā)展,大約10%的人群最終發(fā)展成活動(dòng)性肺結(jié)核。在結(jié)核分枝桿菌(Mtb)感染的后期,機(jī)體免疫系統(tǒng)由于受到損傷而導(dǎo)致結(jié)核分枝桿菌復(fù)蘇,形成慢性感染性結(jié)核,機(jī)體在長期慢性感染的作用下,主要表現(xiàn)為免疫功能低下。重癥肺結(jié)核病人為何表現(xiàn)為免疫力低下?是否發(fā)生了T細(xì)胞功能耗竭?本研究通過分析臨床肺結(jié)核病人外周血T細(xì)胞功能耗竭相關(guān)的幾組功能學(xué)指標(biāo),來探討慢性肺結(jié)核病人發(fā)生T細(xì)胞耗竭的機(jī)制。目的為分析慢性肺結(jié)核病人免疫功能低下的原因,探討結(jié)核分枝桿菌在人體內(nèi)的持續(xù)感染是否造成T細(xì)胞功能耗竭,研究持續(xù)痰菌陽性的空洞性肺結(jié)核病人T細(xì)胞功能的變化。方法:抽取蘭州市肺科醫(yī)院正在住院治療的肺結(jié)核病人51例及健康志愿者16例,分離外周血單個(gè)核細(xì)胞(peripheral blood mononuclear cells,PBMCs)。1,利用酶聯(lián)免疫斑點(diǎn)試驗(yàn)(ELISPOT)檢測外周血T淋巴細(xì)胞經(jīng)抗原ESAT-6和CFP-10刺激后IFN-γ的分泌水平;2,利用ELISA技術(shù)檢測T淋巴細(xì)胞培養(yǎng)基上清中IL-2的分泌水平;3,在結(jié)核菌素純蛋白衍生物(PPD)的刺激下培養(yǎng)PBMCs,用流式細(xì)胞術(shù)分析外周血T細(xì)胞的增殖能力;4,檢測CD4~+、CD8~+T細(xì)胞的數(shù)目,以及CD4~+、CD8~+T細(xì)胞表面免疫抑制相關(guān)分子T細(xì)胞免疫球蛋白粘蛋白分子3(T cell immunoglobulin mucin domain containingmolecules 3,TIM-3)的表達(dá);5,調(diào)取各組病人同一時(shí)期外周血血象,分析外周血中紅細(xì)胞、血紅蛋白、白細(xì)胞、血小板以及單個(gè)核細(xì)胞結(jié)果;6,通過分析病人性別、年齡、病程、初(復(fù))治、痰抗酸染色、肺部影像學(xué)檢查結(jié)果與T細(xì)胞耗竭相關(guān)指標(biāo)的關(guān)系,來探究幾種類型的慢性肺結(jié)核病人發(fā)生T細(xì)胞耗竭的情況。結(jié)果:本實(shí)驗(yàn)室結(jié)合前期工作的基礎(chǔ),得出與T細(xì)胞耗竭相關(guān)的幾個(gè)因素是:抗酸染色、空洞情況、病程長短。以相關(guān)的幾個(gè)因素將51例肺結(jié)核病人和16例健康志愿者分成4組,即健康對(duì)照組(HD組)、痰抗酸染色陰性肺結(jié)核病人組(N-TB組)、痰抗酸染色陽性的非空洞性肺結(jié)核病人組(PNC-TB組)以及痰抗酸染色陽性空洞性肺結(jié)核病人組(PC-TB組)。1,相對(duì)于健康對(duì)照組,痰抗酸染色陰性結(jié)核病人組及痰抗酸染色陽性的非空洞性結(jié)核病人組的T細(xì)胞增殖能力及分泌IFN-γ能力顯著增高(P0.05);2,所有肺結(jié)核病人組的IL-2表達(dá)水平較健康對(duì)照組明顯下降(P0.05),但肺結(jié)核病人各組之間無顯著性差異(P0.05);3,與上述兩組相比,痰抗酸染色陽性空洞性肺結(jié)核病人組T細(xì)胞增殖能力和分泌IFN-γ能力顯著降低(P0.05);4,所有肺結(jié)核病人組TIM-3的表達(dá)水平較健康對(duì)照組顯著增高(P0.05),但在肺結(jié)核病人組之間的差異不明顯(P0.05);5,痰抗酸染色陽性空洞型肺結(jié)核人CD4~+、CD4~+TIM-3~+T細(xì)胞的數(shù)目有所下降,但差異尚不顯著(P0.05),可能與樣本量較小有關(guān);6,痰抗酸染色陽性空洞型肺結(jié)核病人血小板數(shù)目較其他各組出現(xiàn)減少,差異有統(tǒng)計(jì)學(xué)意義(P0.05),各組病人外周血中紅細(xì)胞、血紅蛋白、白細(xì)胞以及單個(gè)核細(xì)胞之間無顯著性差異。結(jié)論:1,TIM-3可能作用于肺結(jié)核病發(fā)展的整個(gè)過程;2,T細(xì)胞分泌IL-2的能力在肺結(jié)核發(fā)展的早期就開始下降;3,肺結(jié)核病人發(fā)生T細(xì)胞耗竭與抗酸染色、空洞情況、病程長短幾個(gè)因素相關(guān);4,本研究證實(shí)持續(xù)痰菌陽性的空洞性肺結(jié)核病人T細(xì)胞功能出現(xiàn)耗竭,提示人體內(nèi)大量結(jié)核分枝桿菌持續(xù)感染可導(dǎo)致T細(xì)胞功能耗竭。結(jié)核病是由結(jié)核分枝桿菌引起的一種慢性傳染病,它不僅可以引起肺結(jié)核也可以肺外結(jié)核,結(jié)核分枝桿菌在宿主體內(nèi)長期持續(xù)存在,損害宿主的免疫功能。類似于HBV、HCV、HIV等病毒性疾病持續(xù)感染所致的T細(xì)胞耗竭,結(jié)核分枝桿菌持續(xù)感染所致的T細(xì)胞功能耗竭越來越受到重視。發(fā)生耗竭的T細(xì)胞主要表現(xiàn)是細(xì)胞表面抑制性受體增加,細(xì)胞增殖能力下降,細(xì)胞毒作用喪失以及細(xì)胞因子分泌能力降低。結(jié)核病患者一旦發(fā)生T細(xì)胞耗竭,機(jī)體表現(xiàn)為免疫功能低下,疾病持續(xù)惡化,很難恢復(fù)。為逆轉(zhuǎn)結(jié)核病T細(xì)胞耗竭,恢復(fù)機(jī)體免疫功能,本研究構(gòu)建動(dòng)物模型來驗(yàn)證兩種逆轉(zhuǎn)T細(xì)胞耗竭藥物的作用。目的:研究結(jié)核分枝桿菌抗原持續(xù)刺激致T細(xì)胞功能耗竭的機(jī)制,探究補(bǔ)腎健脾方和二甲雙胍逆轉(zhuǎn)T細(xì)胞功能耗竭的作用。方法:將3周齡的實(shí)驗(yàn)動(dòng)物隨機(jī)分為5組:正常對(duì)照組、抗原短暫免疫組、免疫耗竭未治療組、免疫耗竭補(bǔ)腎健脾解毒方組、免疫耗竭二甲雙胍治療組。實(shí)驗(yàn)第1周利用BCG初免,PPD(結(jié)核菌素純蛋白衍化物蛋白)持續(xù)刺激C57BL/6小鼠,模擬結(jié)核分枝桿菌抗菌抗原在病人體內(nèi)持續(xù)存在所造成慢性感染的過程,構(gòu)建T細(xì)胞功能耗竭模型。從第7周開始,給予免疫耗竭二甲雙胍治療組飲水中給藥治療至第26周,從第24周開始,給予補(bǔ)腎健脾解毒方組小鼠灌胃治療至第26周。治療完成后檢測各組小鼠細(xì)胞免疫水平,包括利用流式細(xì)胞術(shù)檢測脾臟CD4~+和CD8~+T細(xì)胞PD-1的表達(dá)水平、CD4~+和CD8~+T細(xì)胞的數(shù)目;利用ELISA檢測脾臟淋巴細(xì)胞分泌IL-2和IFN-γ的水平;利用肺臟BCG攻毒實(shí)驗(yàn)檢測抗感染能力;利用流式細(xì)胞術(shù)檢測造血干細(xì)胞占小鼠骨髓有核細(xì)胞的比例。結(jié)果:與抗原短暫刺激組相比,免疫耗竭未治療組CD4~+和CD8~+T細(xì)胞數(shù)目顯著下降(P0.05),細(xì)胞表面PD-1的表達(dá)水平顯著增高,差異有統(tǒng)計(jì)學(xué)意義(P0.01);脾淋巴細(xì)胞分泌細(xì)胞因子IL-2、IFN-γ的水平明顯降低,差異有統(tǒng)計(jì)學(xué)意義(P0.01);小鼠抗感染的能力顯著下降,差異有統(tǒng)計(jì)學(xué)意義(P0.01);說明PPD抗原持續(xù)刺激致T細(xì)胞耗竭模型構(gòu)建成功。經(jīng)補(bǔ)腎健脾方治療后,小鼠脾臟CD4~+T細(xì)胞表面PD-1的表達(dá)水平顯著降低,差異有統(tǒng)計(jì)學(xué)意義(P0.01),CD4~+和CD8~+T細(xì)胞數(shù)目得到明顯恢復(fù)(P0.05);小鼠脾臟T淋巴細(xì)胞分泌IL-2、IFN-γ的水平明顯增高,差異有統(tǒng)計(jì)學(xué)意義(P0.01);小鼠抗BCG感染的能力顯著增強(qiáng),差異有統(tǒng)計(jì)學(xué)意義(P0.01);小鼠脾臟的炎癥反應(yīng)明顯減輕,差異有統(tǒng)計(jì)學(xué)意義(P0.05)。經(jīng)二甲雙胍干預(yù)后,脾CD4~+T細(xì)胞PD-1的表達(dá)顯著性降低,差異有統(tǒng)計(jì)學(xué)意義(P0.01);脾淋巴細(xì)胞分泌IL-2和IFN-γ的水平明顯增高,差異有統(tǒng)計(jì)學(xué)意義(P0.01);小鼠抗感染的能力顯著性增強(qiáng),差異有統(tǒng)計(jì)學(xué)意義(P0.01)。結(jié)論:1,抗原PPD持續(xù)刺激可致T細(xì)胞發(fā)生耗竭;2,補(bǔ)腎健脾方能逆轉(zhuǎn)抗原持續(xù)刺激導(dǎo)致的小鼠T細(xì)胞功能耗竭,可能為臨床治療結(jié)核病T細(xì)胞功能耗竭提供參考;3,二甲雙胍對(duì)T細(xì)胞功能耗竭的進(jìn)展有干預(yù)作用,提示患有二型糖尿病或者空腹血糖受損的肺結(jié)核病人口服二甲雙胍的必要性。
[Abstract]:Worldwide, the prevalence and fatality of tuberculosis are very high, especially in developing countries such as China and India. Tuberculosis is a heavy burden to society and individuals. In the early stages of Mycobacterium tuberculosis, most people can prevent further development of tuberculosis through their own immunity, and about 10% of the population end up. It is developed into active tuberculosis. In the late stage of Mycobacterium tuberculosis (Mtb) infection, the immune system caused the recovery of Mycobacterium tuberculosis and the formation of chronic infectious tuberculosis. The main manifestations of the body are low immune function under the effect of chronic chronic infection. Why are the patients with severe pulmonary tuberculosis manifested as low immunity? In this study, the mechanism of the depletion of T cells in the patients with chronic pulmonary tuberculosis was investigated by analyzing several functional indexes related to the depletion of the function of T cells in the peripheral blood of the patients with clinical pulmonary tuberculosis. The purpose of this study was to analyze the causes of the low immune function of the patients with chronic pulmonary tuberculosis and to explore the holding of Mycobacterium tuberculosis in the human body. Whether continuous infection causes T cell function depletion and study the changes of T cell function in patients with persistent phlegm positive cavitary pulmonary tuberculosis. Methods: 51 cases of pulmonary tuberculosis patients in Lanzhou lung hospital and 16 healthy volunteers were selected, and the peripheral blood mononuclear cells (peripheral blood mononuclear cells, PBMCs).1 were isolated and the enzyme was used. The secretory level of IFN- gamma in peripheral blood T lymphocytes stimulated by antigen ESAT-6 and CFP-10 was detected by ELISPOT. 2, the secretion level of IL-2 in the supernatant of T lymphocyte culture was detected by ELISA technique; 3, PBMCs was cultured under the stimulation of Purified Protein Derivative of Tuberculin (PPD), and the increase of T cells in peripheral blood was analyzed by flow cytometry. Colonization; 4, the number of CD4~+, CD8~+T cells, and the expression of T cell immunoglobulin 3 (T cell immunoglobulin mucin domain containingmolecules 3, TIM-3), and the expression of CD4~+, CD8~+T cell surface immunosuppressive related molecules; 5, the blood hemogram of the same period of the same period of the patients, the red and blood eggs of the peripheral blood were analyzed. White, white blood cells, platelets and mononuclear cells; 6, by analyzing the relationship between sex, age, course of disease, initial (complex) treatment, sputum acid staining, lung imaging findings and T cell depletion related indicators to explore the depletion of T cells in several types of chronic tuberculosis patients. Results: this laboratory combined with previous work. Several factors related to the depletion of T cells were: acid stain, cavity and length of disease. 51 cases of tuberculosis patients and 16 healthy volunteers were divided into 4 groups, that is, healthy control group (group HD), sputum acid negative staining negative pulmonary tuberculosis group (group N-TB), phlegm positive non cavity pulmonary tuberculosis The group (group PNC-TB) and the sputum acid positive cavitary pulmonary tuberculosis group (group PC-TB).1, compared with the healthy control group, the T cell proliferation ability and the secretion of IFN- gamma in the group of phlegm negative acid negative tuberculosis patients and phlegm positive non cavity tuberculosis patients were significantly increased (P0.05); 2, IL-2 table of all pulmonary tuberculosis patients group. There was a significant decrease in the level of reaching the level of the healthy control group (P0.05), but there was no significant difference between the pulmonary tuberculosis patients (P0.05). 3, compared with the two groups, the T cell proliferation ability and the secretion of IFN- gamma in the phlegm positive cavitary pulmonary tuberculosis patients were significantly lower (P0.05); 4, the expression level of TIM-3 in all patients with tuberculosis was more than that of the healthy control group. There was a significant increase (P0.05), but the difference between the patients with pulmonary tuberculosis was not significant (P0.05); 5, the number of CD4~+ and CD4~+TIM-3~+T cells in the phlegm positive cavitary pulmonary tuberculosis decreased, but the difference was not significant (P0.05), which may be related to the small sample size; 6, the number of platelets in the phlegm positive cavitary pulmonary tuberculosis patients was more than that of the others. There was no significant difference in each group (P0.05). There was no significant difference between the peripheral blood red blood cells, hemoglobin, leukocyte and mononuclear cells in the peripheral blood of each group. Conclusion: 1, TIM-3 may act on the whole process of pulmonary tuberculosis development; 2, the ability of T cells to secrete IL-2 begins to decline in the early stage of tuberculosis development; 3, tuberculosis. T cell depletion was associated with a number of factors associated with acid resistance, cavity conditions, and duration of the disease. 4, this study confirmed the depletion of T cell function in patients with persistent phlegm positive cavitary tuberculosis, suggesting that the persistent infection of a large number of Mycobacterium tuberculosis in the human body can lead to the exhaustion of T cells. Tuberculosis is caused by Mycobacterium tuberculosis. Chronic infectious diseases can not only cause tuberculosis but also extrapulmonary tuberculosis. Mycobacterium tuberculosis persists in the host for a long time and damages the immune function of the host. It is similar to the depletion of T cells caused by persistent infection of viral diseases such as HBV, HCV, HIV, and the depletion of T cells caused by the persistent infection of Mycobacterium tuberculosis. The main manifestations of the depleted T cells are the increase of the cell surface inhibitory receptor, the decline of cell proliferation, the loss of cytotoxic effect and the decrease of cytokine secretion ability. Once the patients with tuberculosis occur T cells exhaustion, the body is immune to low immune function, and the disease continues to deteriorate, it is difficult to restore the exhaustion of tuberculosis T cells. To restore the immune function of the body, this study constructs an animal model to verify the effect of two kinds of reverse T cell exhaustion drugs. Objective: To study the mechanism of T cell depletion by the continuous stimulation of Mycobacterium tuberculosis, and to explore the role of the kidney invigorating spleen recipe and metformin in reversing the function depletion of T cells. Methods: the experimental animals of 3 weeks of age were randomly divided into two groups. The 5 groups: the normal control group, the antigen transient immune group, the immune exhaustion untreated group, the immune exhausted invigorating kidney invigorating spleen and the detoxification group, the immune exhaustion metformin treatment group. The experiment first weeks using BCG primordial immunity and PPD (tuberculin pure protein derivative protein) continuously stimulated C57BL/6 mice, and simulated the persistent presence of Mycobacterium tuberculosis antigenic antigen in the patient's body. In the process of chronic infection, the function depletion model of T cells was constructed. From seventh weeks, the treatment group of metformin in the treatment group of the immune depleted metformin treatment group was treated for twenty-sixth weeks. From the twenty-fourth week, the mice were given the kidney invigorating spleen and the spleen detoxification group for twenty-sixth weeks. After the treatment was completed, the cell immune level of each group was detected, including the use of flow. The expression level of PD-1, the number of CD4~+ and CD8~+T cells, the number of CD4~+ and CD8~+T cells, the level of the secretion of IL-2 and IFN- in the spleen lymphocytes were detected by ELISA, and the anti infective ability of the spleen lymphocytes to detect the secretion of IL-2 and IFN- gamma; the detection of anti infection ability by the lung BCG attack test; the ratio of hematopoietic stem cells to the marrow nucleated cells in mice was detected by flow cytometry. Compared with the primary transient stimulation group, the number of CD4~+ and CD8~+T cells in the untreated group was significantly decreased (P0.05), and the expression level of PD-1 on the cell surface was significantly higher, the difference was statistically significant (P0.01); the level of cell factor IL-2, IFN- gamma decreased significantly (P0.01), and the ability of anti infection in mice was significant (P0.01). The difference was statistically significant (P0.01), indicating that the T cell depletion model was constructed successfully by the continuous stimulation of PPD antigen. After the treatment of kidney invigorating spleen, the expression level of PD-1 on the surface of CD4~+T cells in spleen of mice decreased significantly (P0.01), the number of CD4~+ and CD8~+T cells recovered significantly (P0.05), and the T lymph nodes of mouse spleen were fine. The level of IL-2 and IFN- gamma increased significantly, the difference was statistically significant (P0.01), the ability of mice to resist BCG infection was significantly enhanced, the difference was statistically significant (P0.01), the inflammatory response of spleen in mice was significantly reduced, and the difference was statistically significant (P0.05). The expression of PD-1 in spleen CD4~+T cells decreased significantly after two metformin, and the difference had a significant difference. Study significance (P0.01); the secretion of IL-2 and IFN- gamma in spleen lymphocytes increased significantly, the difference was statistically significant (P0.01); the ability of anti infection in mice increased significantly (P0.01). Conclusion: 1, the continuous stimulation of antigen PPD can cause depletion of T cells; 2, the recipe for invigorating the kidney and invigorating the spleen can reverse the T fines caused by the continuous antigen stimulation of the antigen. The depletion of cell function may provide a reference for the clinical treatment of T cell depletion of TB cells; 3, metformin has an intervention in the progress of T cell depletion, suggesting the necessity of oral metformin in patients with type two diabetes or impaired fasting blood glucose.

【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】：2017
【分類號(hào)】：R521;R-332

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