本文選題：慢性阻塞性肺疾病 + 淋巴細(xì)胞趨化因子��； 參考：《遵義醫(yī)學(xué)院》2013年碩士論文

【摘要】：目的：研究淋巴細(xì)胞趨化因子(Lymphotactin,XCL1)在慢性阻塞性肺疾病患者外周血中的表達(dá)水平,并與COPD患者肺功能下降程度的相關(guān)性,及干預(yù)前后IL-2、T細(xì)胞及其表面Fas、FasL表達(dá)水平的變化,探討XCL1對(duì)COPD患者慢性炎癥的調(diào)控機(jī)制。 方法：COPD急性加重期(AECOPD)患者13例,均來(lái)自龍崗中心醫(yī)院2012年8月至2012年12月呼吸內(nèi)科住院患者；穩(wěn)定期患者13例,均為急性加重期患者經(jīng)治療后出院病情穩(wěn)定至少2周者；健康對(duì)照組選用門診體檢性別、年齡與病例組相配的肺功能正常者。清晨空腹抽取外周靜脈血用于分離血清及T淋巴細(xì)胞,經(jīng)分離后的T淋巴細(xì)胞分為2組,接種于24孔細(xì)胞培養(yǎng)板,其中一板加入重組人淋巴細(xì)胞趨化因子(Recombinant Human Lymphotactin,RhXCL1)(干預(yù)組),另一板加入等量細(xì)胞培養(yǎng)液(未干預(yù)組),培養(yǎng)24小時(shí),采用酶聯(lián)免疫吸附法(Enzyme linked immunosorbent assay,ELISA)分別檢測(cè)血清及細(xì)胞培養(yǎng)上清液中的XCL1、白細(xì)胞介素2(Interleukin-2,IL-2);采用流式細(xì)胞儀檢測(cè)細(xì)胞培養(yǎng)液中的T淋巴細(xì)胞亞群CD4+、 CD8+及其表面的Fas、 FasL的表達(dá)水平。 結(jié)果： 1、外周血XCL1的表達(dá)及與FEVl%pred、IL-2的相關(guān)性： ①AECOPD及穩(wěn)定期患者外周血中的XCL1的表達(dá)均高于健康對(duì)照組,差異有統(tǒng)計(jì)學(xué)意義(P0.05),AECOPD患者又高于穩(wěn)定期患者,結(jié)果有顯著性差異(P0.05)。 ②AECOPD患者外周血中XCL1的表達(dá)水平與FEVl%pred呈負(fù)相關(guān),與IL-2的表達(dá)水平在急性期呈正相關(guān),在穩(wěn)定期無(wú)明顯相關(guān)性。 2、T淋巴細(xì)胞培養(yǎng)液中各指標(biāo)比較及與XCL1的相關(guān)性： ①干預(yù)組COPD患者(包括急性期與穩(wěn)定期)的T細(xì)胞培養(yǎng)液中XCL1、CD4+-Fas、 CD4+-FasL、CD8+-Fas. CD8+-FasL的表達(dá)均高于未干預(yù)組,而IL-2表達(dá)減少,結(jié)果有顯著性差異(P0.05)。 ②干預(yù)組COPD患者(包括急性期及穩(wěn)定期)的T細(xì)胞培養(yǎng)液中CD4+百分比降低、CD8+百分比升高,CD4+/CD8+降低,與未干預(yù)組相比,結(jié)果有顯著性差異(P0.05)。 ③干預(yù)組COPD患者(包括急性期與穩(wěn)定期)的T細(xì)胞培養(yǎng)液中,XCL1的表達(dá)與CD4+-Fas、CD4+-FasL、CD8+-Fas、CD8+-FasL的表達(dá)呈正相關(guān),與IL-2的表達(dá)及CD4+/CD8+呈負(fù)相關(guān)。 結(jié)論： 1、XCL1在AECOPD及穩(wěn)定期患者外周血中的表達(dá)水平均較健康對(duì)照組明顯升高,且急性加重期高于穩(wěn)定期,并與肺功能指標(biāo)FEV1%pred呈負(fù)相關(guān),在干預(yù)組T細(xì)胞培養(yǎng)液中,CD4+-Fas、CD4+-FasL、CD8+-Fas、CD8+-FasL的表達(dá)均有不同程度增加,且與XCL1的表達(dá)呈正相關(guān),提示XCL1參與了COPD的炎癥過(guò)程,其參與炎癥反應(yīng)的機(jī)制可能是通過(guò)促進(jìn)Fas、FasL的表達(dá),導(dǎo)致CD4+T細(xì)胞的凋亡,進(jìn)行性破壞CD4+、CD8+之間的平衡發(fā)揮效應(yīng)。 2. COPD患者外周血T細(xì)胞經(jīng)干預(yù)培養(yǎng)后,IL-2表達(dá)水平降低,與XCL1呈負(fù)相關(guān),提示XCL1可能引起IL-2表達(dá)水平降低,間接導(dǎo)致自身反應(yīng)性淋巴細(xì)胞增生或免疫功能紊亂或低下,可能是導(dǎo)致COPD氣道炎癥持續(xù)存在的原因之一。
[Abstract]:Objective: To study the expression of Lymphotactin (XCL1) in peripheral blood of patients with chronic obstructive pulmonary disease, the correlation with the degree of pulmonary function decline in COPD patients, and the changes of IL-2, T cells and their Fas and FasL expression levels before and after intervention, and to explore the regulation mechanism of XCL1 on chronic inflammation in patients with COPD.
Methods: 13 patients with acute exacerbation of COPD (AECOPD) were hospitalized in the respiratory department of Longgang Central Hospital from August 2012 to December 2012, and 13 patients in the stable period were all patients who had been discharged from the hospital after treatment for at least 2 weeks after treatment. Normal subjects. Peripheral venous blood was extracted from the abdomen in the morning to separate serum and T lymphocytes. The separated T lymphocytes were divided into 2 groups and inoculated into 24 cell culture plates, one of which was added to the recombinant human lymphocyte chemoattractant factor (Recombinant Human Lymphotactin, RhXCL1), and the other was added to the same amount of cell culture solution (unprepared). Enzyme linked immunosorbent assay (ELISA) was used to detect XCL1 and interleukin 2 (Interleukin-2, IL-2) in serum and cell culture supernatant for 24 hours, and the T lymphocyte subgroup CD4+, CD8+ and surface Fas, and the expression level were detected by flow cytometry.
Result錛，

本文編號(hào)：1855670