發(fā)布時(shí)間：2018-05-25 02:04

  本文選題：IL13 + CCL5�。� 參考：《華中科技大學(xué)》2012年碩士論文

【摘要】：研究背景 目前哮喘發(fā)病率呈現(xiàn)上升趨勢(shì)，但是哮喘的發(fā)病機(jī)制尚未完全闡明。哮喘是以氣道高反應(yīng)性、粘液分泌增多和慢性嗜酸性粒細(xì)胞炎癥為特點(diǎn)。有些報(bào)道已證實(shí)主要在哮喘患者氣道上皮細(xì)胞和單核細(xì)胞中，一些趨化因子RANTES,MCP-3,MCP-4,eotaxin-1andeotaxin-2等的mRNA表達(dá)是增加的。趨化因子是8-10kDa的小分子細(xì)胞因子，根據(jù)每個(gè)蛋白分子一個(gè)或兩個(gè)半胱氨酸殘基在N末端的位置可以分為四類，即，CXC,CC,C,和CXXXC。許多CC類趨化因子是由氣道上皮細(xì)胞產(chǎn)生的。IL13可以誘導(dǎo)上皮細(xì)胞CCL11(eotaxin),CCL24(eotaxin-2),andCCL26(eotaxin-3)的表達(dá)，且這些因子的表達(dá)在哮喘者是增加的。這些CC類趨化因子是嗜酸性粒細(xì)胞和嗜堿性細(xì)胞表面CCR受體的選擇性激動(dòng)劑。 哮喘是以TH2細(xì)胞調(diào)節(jié)為主，分泌的細(xì)胞因子與IL4/5/9/13,雖然都與哮喘相關(guān)，但是IL13是現(xiàn)在認(rèn)為最關(guān)鍵的因子。白介素13是由TH2型細(xì)胞分泌的分子量為12kDa多效能分子，位于常染色體5q31上。白介素13是富含嗜酸性粒細(xì)胞、淋巴細(xì)胞和巨噬細(xì)胞炎癥、粘液上皮化生、組織纖維化和基底重塑強(qiáng)有力的刺激劑。白介素13能夠刺激哮喘相關(guān)的許多細(xì)胞，例如B淋巴細(xì)胞、肥大細(xì)胞、嗜酸性粒細(xì)胞、肺泡上皮細(xì)胞、成纖維細(xì)胞和氣道平滑肌細(xì)胞。一些實(shí)驗(yàn)也證明，重組白介素13的應(yīng)用或是肺中白介素13的過(guò)表達(dá)可以產(chǎn)生哮喘樣的氣道炎癥和氣道重塑。許多實(shí)驗(yàn)證實(shí)白介素13在哮喘中是過(guò)表達(dá)的，且與哮喘的特征TH2細(xì)胞炎癥和氣道重塑的發(fā)病機(jī)制相關(guān)。因此，我們用IL13刺激氣道上皮細(xì)胞，模擬哮喘樣作用。 人intelectin(ITLN)是一種分泌性的糖蛋白，由295個(gè)氨基酸和N端寡糖組成，它的基本結(jié)構(gòu)單位是二硫鍵連接40kDa多肽成的120kDa的三聚體�？煞譃閕ntelectin-1和2。人intelectin也被稱作甘油磷酸肌醇連接的轉(zhuǎn)鐵蛋白受體、血管內(nèi)皮細(xì)胞凝集素或網(wǎng)膜素。人ITLN基因位于染色體1q21.3上，含有8個(gè)外顯子，，且人intelectin的mRNA表達(dá)于心臟、小腸、結(jié)腸和胸腺。屬于凝集素類，能夠識(shí)別特定的細(xì)菌壁組分，而不被其他凝集素所識(shí)別。所熟知的是它在小腸的潘氏細(xì)胞和分泌或是杯狀細(xì)胞表達(dá)。最近，也觀察到在氣道上皮細(xì)胞分泌細(xì)胞也有表達(dá)�？梢宰R(shí)別存在于細(xì)菌、真菌和原蟲壁上右旋戊糖和呋喃半乳糖殘基，但在哺乳動(dòng)物在不然，說(shuō)明intelectin在抗原識(shí)別中起重要作用。Intelectin-1在小鼠小腸暴露于線旋毛蟲后，表達(dá)是上調(diào)的，其同種型intelectin-2在小腸上皮細(xì)胞也被誘導(dǎo)。Intelectin-1是一個(gè)TH2細(xì)胞調(diào)節(jié)的抗菌蛋白，在哮喘患者支氣管上皮細(xì)胞中intelectin-1的基因表達(dá)水平是上調(diào)的，與IL13的表達(dá)上調(diào)相關(guān)。 第一部分Intelectin-1在IL13誘導(dǎo)的氣道上皮細(xì)胞株A549和16HBE中炎性細(xì)胞因子表達(dá)中的作用 目的：探討intelectin-1基因在人肺泡/氣道上皮細(xì)胞分泌炎性因子中的作用。 方法：實(shí)驗(yàn)用兩種細(xì)胞系A(chǔ)549和16HBE。分為轉(zhuǎn)染高表達(dá)質(zhì)粒分組為：（A）正常對(duì)照組（B）IL13組（C）轉(zhuǎn)染人ITLN1質(zhì)粒組；轉(zhuǎn)染干擾質(zhì)粒分組：（A）正常對(duì)照組+空質(zhì)粒組（B）IL13+空質(zhì)粒組（C）IL13+Itln1-shRNA質(zhì)粒組。通過(guò)RealtimePCR方法檢測(cè)intelectin-1，CCL5和IL6mRNA的表達(dá)。ELISA方法檢測(cè)細(xì)胞上清液中相應(yīng)因子的蛋白水平表達(dá)。地塞米松干預(yù)細(xì)胞：①對(duì)照組+DMSO②IL13+DMSO③DEX100+IL13，然后通過(guò)RealtimePCR檢測(cè)細(xì)胞因子ITLN1,CCL5和IL6mRNA的表達(dá)。 結(jié)果：A549細(xì)胞中Intelectin-1，CCL5,IL6mRNA的表達(dá)水平，人ITLN1組和IL13組較對(duì)照組均明顯升高，p0.05。而16HBE細(xì)胞Intelectin-1，CCL5,IL6mRNA的表達(dá)水平，人ITLN1組較對(duì)照組明顯增高，P0.05均有統(tǒng)計(jì)學(xué)意義；IL13組較對(duì)照組Intelectin-1，IL6mRNA表達(dá)水平增高，P0.05；但是IL13組較對(duì)照組CCL5mRNA表達(dá)水平有增高趨勢(shì)，但是未有統(tǒng)計(jì)意義。細(xì)胞A549和16HBE轉(zhuǎn)染人ITLN1-shRNA質(zhì)粒后，A549和16HBE細(xì)胞系：IL13+人ITLN1shRNA質(zhì)粒組較IL13組intelectin-1,CCL5和IL6的表達(dá)明顯下降，P0.05，均有統(tǒng)計(jì)學(xué)意義。ELISA方法檢測(cè)蛋白水平：高表達(dá)實(shí)驗(yàn)，人ITLN質(zhì)粒組與對(duì)照組相比，IL6,CCL5的蛋白表達(dá)水平明顯升高P0.05。干擾實(shí)驗(yàn)組：IL13組較對(duì)照組，CCL5和IL6的蛋白表達(dá)水平明顯升高P0.05；IL13+ITLN1-shRNA組較IL13組，CCL5和IL6的蛋白表達(dá)水平明顯降低P0.05。在A549細(xì)胞，地塞米松+IL13組較IL13組，ITLN1,CCL5和IL6明顯減少的，P0.05;在16HBE細(xì)胞，地塞米松組較IL13組，ITLN1,CCL5和IL6均有顯著下降，并p0.05,均有統(tǒng)計(jì)學(xué)意義。 結(jié)論：轉(zhuǎn)入人ITLN1高表達(dá)質(zhì)粒后，成功的促使細(xì)胞intelectin-1mRNA的高表達(dá)。一同檢測(cè)的因子CCL5和IL6的mRNA和蛋白表達(dá)水平也相應(yīng)的升高，可能與intelectin-1的表達(dá)升高有關(guān)。轉(zhuǎn)染人ITLN1干擾質(zhì)粒后，抑制了intelectin-1mRNA的表達(dá),一同檢測(cè)的因子CCL5和IL6的mRNA和蛋白表達(dá)水平也相應(yīng)的降低。Intelectin-1的表達(dá)可能抑制了CCL5和IL6的表達(dá)。糖皮質(zhì)激素可以抑制A549和16HBE細(xì)胞中ITLN1,CCL5和IL6的基因表達(dá)。由此得出，Intelectin-1在IL-13誘導(dǎo)的氣道上皮細(xì)胞中炎性細(xì)胞因子CCL5和IL-6的表達(dá)中有重要的作用。 第二部分ERK信號(hào)通路在intelectin-1介導(dǎo)的氣道上皮細(xì)胞炎性細(xì)胞因子CCL5和IL6表達(dá)中的作用 目的：研究探討intelectin-1參與氣道上皮細(xì)胞中炎性細(xì)胞因子CCL5和IL-6表達(dá)的機(jī)制。 方法：用IL-13和PD98059分別干預(yù)人肺上皮細(xì)胞株A549和16HBE細(xì)胞。PD98059實(shí)驗(yàn)分組(1)對(duì)照組，(2)IL-13組，(3)IL-13+PD98059組。然后用RealTimePCR方法檢測(cè)細(xì)胞因子CCL5和IL6的mRNA的表達(dá)。轉(zhuǎn)染干擾質(zhì)粒分組：（A）正常對(duì)照組+空質(zhì)粒組（B）IL13+空質(zhì)粒組（C）IL13+humanITLN1shRNA質(zhì)粒組，通過(guò)RNA干擾的方法抑制IL-13誘導(dǎo)的intelectin-1表達(dá)后，用Western-Blot檢測(cè)intelectin-1,ERK1/2和P-ERK1/2蛋白水平的變化。 結(jié)果：用PD98059干預(yù)IL13刺激的A549和16HBE細(xì)胞后,CCL5和IL6的mRNA表達(dá)水平，IL13+PD98059組較IL13組明顯降低，P0.05。轉(zhuǎn)染humanITLN1shRNA質(zhì)粒后，intelectin-1和P-ERK1/2蛋白表達(dá)水平，IL-13組較對(duì)照組升高，P0.05；IL-13+shRNA組中intelectin-1和P-ERK1/2蛋白表達(dá)較IL-13組降低，P0.05。 結(jié)論：ERK1/2的一種抑制劑PD98059，可以阻滯IL-13誘導(dǎo)的CCL5和IL6在A549和16HBE細(xì)胞中的表達(dá)。而且IL-13的刺激增加了ERK1/2磷酸化以及intelectin-1蛋白表達(dá)，但HumanITLLN1-shRNA質(zhì)粒轉(zhuǎn)染抑制了IL-13誘導(dǎo)的intelectin-1蛋白表達(dá)及ERK1/2磷酸化。這些數(shù)據(jù)顯示了ERK1/2通路可以調(diào)節(jié)IL-13誘導(dǎo)CCL5和IL6的表達(dá)，Intelectin-1基因參與了IL-13誘導(dǎo)ERK1/2在A549和16HBE細(xì)胞的激活表達(dá)。因此我們可以這樣認(rèn)為，Intelectin-1基因可能通過(guò)激活ERK1/2信號(hào)通路，參與IL-13誘導(dǎo)的CCL5和IL6的表達(dá)。
[Abstract]:Research background
The incidence of asthma is on the rise, but the pathogenesis of asthma has not been fully elucidated. Asthma is characterized by airway hyperresponsiveness, increased mucus secretion and chronic eosinophil inflammation. Some reports have been confirmed mainly in airway epithelial cells and mononuclear cells in asthmatic patients, and some chemokines RANTES, MCP-3, MCP-4, eotax. The expression of mRNA in in-1andeotaxin-2 is increased. Chemokine is a small molecular cytokine of 8-10kDa. According to each protein molecule, one or two cysteine residues can be divided into four types at the N terminal position, that is, CXC, CC, C, and CXXXC. many CC chemokines are produced by.IL13 that can induce epithelial cell CCL11. (eotaxin), the expression of CCL24 (eotaxin-2), andCCL26 (eotaxin-3), and the expression of these factors is increased in the patients with asthma. These CC chemokines are selective agonists of the eosinophil and the surface of the basophil on the surface of the CCR receptor.
Asthma is mainly regulated by TH2 cells, secreted cytokines and IL4/5/9/13, which are all associated with asthma, but IL13 is now considered the most critical factor. Interleukin 13 is a 12kDa multipotent molecule secreted by TH2 cells, located on the autosomal 5q31. Interleukin 13 is rich in eosinophils, lymphocytes and mega - macrophages. Cell inflammation, mucous epithelialization, tissue fibrosis and a strong stimulant for the remodeling of the base. Interleukin 13 stimulates many of the cells associated with asthma, such as B lymphocytes, mast cells, eosinophils, alveolar epithelial cells, fibroblasts and airway smooth muscle cells. Some experiments have also proved that the application of recombinant interleukins 13 is or is The overexpression of interleukin 13 in the lung can produce asthma like airway inflammation and airway remodeling. Many experiments have confirmed that interleukin 13 is overexpressed in asthma and is associated with the pathogenesis of TH2 cell inflammation and airway remodeling in asthma. Therefore, we use IL13 to stimulate airway epithelial cells to simulate asthma like effects.
Human intelectin (ITLN) is a secretory glycoprotein consisting of 295 amino acids and N terminal oligosaccharides. Its basic structural unit is the 120kDa trimer of the two sulfur bonds connected to the 40kDa polypeptide. It can be divided into intelectin-1 and 2. intelectin, also known as the transferrin receptor of the glycerol phosphoric inositol connection, vascular endothelial cell agglutinin or omentum The human ITLN gene is located on the chromosome 1q21.3, containing 8 exons, and the mRNA of human intelectin is expressed in the heart, the small intestine, the colon and the thymus. It is a lectin class that recognizes specific bacterial wall components and is not recognized by other lectin. It is known that it is expressed in the small intestine of pans cells and secreted or goblet cells. It is also observed that the secretory cells in the airway epithelial cells are also expressed. It can be identified in bacteria, fungi and protozoan walls of dextran and furan galactose residues, but in mammals, it is indicated that intelectin plays an important role in antigen recognition and.Intelectin-1 is up to up after exposure to Trichinella spiralis in the small intestine of mice. The type of intelectin-2 in the small intestinal epithelial cells is also induced by.Intelectin-1 as an antiseptic protein regulated by TH2 cells. The expression of intelectin-1 gene expression in bronchial epithelial cells of asthmatic patients is up regulated, which is related to the up regulation of IL13 expression.
Part I the role of Intelectin-1 in the expression of inflammatory cytokines in IL13 induced airway epithelial cell lines A549 and 16HBE.
Objective: To investigate the role of intelectin-1 gene in the secretion of inflammatory factors in human alveolar / airway epithelial cells.
Methods: the transfected high expression plasmids were divided into two types of cell lines A549 and 16HBE.: (A) normal control group (B) IL13 group (C) transfected to human ITLN1 plasmid group, and transfected interference plasmid group: (A) normal control group + empty plasmid group (B) IL13+ empty plasmid group (C) IL13+ replication plasmid group. L6mRNA expression.ELISA method was used to detect the protein level of the corresponding factors in the cell supernatant. Dexamethasone intervened cells: (1) the control group was +DMSO (IL13+DMSO) DEX100+IL13, and then the expression of cytokines ITLN1, CCL5 and IL6mRNA were detected by RealtimePCR.
Results: the expression level of Intelectin-1, CCL5 and IL6mRNA in A549 cells was significantly higher in the ITLN1 group and the IL13 group than in the control group. The expression level of p0.05. and 16HBE cells in Intelectin-1, CCL5, IL6mRNA was significantly higher than that in the control group, and the expression level of the group was higher than that in the control group. 05, but the expression level of CCL5mRNA in the IL13 group was higher than that of the control group, but there was no statistical significance. After the transfection of A549 and 16HBE to the ITLN1-shRNA plasmid, the A549 and 16HBE cell lines: the ITLN1shRNA plasmid group of IL13+ man was lower than the IL13 group intelectin-1, and the expression of the protein water was detected by the statistical significance method. In the high expression test, the expression level of IL6 and CCL5 protein in the human ITLN plasmid group was significantly higher than that in the control group. The protein expression level of CCL5 and IL6 in the IL13 group was significantly higher than that in the control group, and the level of CCL5 and IL6 in the IL13+ITLN1-shRNA group was significantly higher than that in the IL13 group, and the level of CCL5 and IL6 protein was significantly lower than that in the IL13 group. In group IL13 compared with group IL13, ITLN1, CCL5 and IL6 were significantly reduced, P0.05, and in 16HBE cells, dexamethasone group was significantly lower than that in IL13 group, ITLN1, CCL5 and IL6 were significantly decreased, and P0.05, all had statistical significance.
Conclusion: after transferring to the high expression plasmid of human ITLN1, the high expression of intelectin-1mRNA is promoted. The mRNA and protein expression level of factors CCL5 and IL6 are also increased, which may be related to the increase of intelectin-1 expression. After transfection of human ITLN1 interference plasmid, the expression of intelectin-1mRNA and the factors to be detected together can be suppressed. MRNA and protein expression levels of CCL5 and IL6 also correspondingly decrease the expression of.Intelectin-1, which may inhibit the expression of CCL5 and IL6. Glucocorticoid can inhibit the gene expression of ITLN1, CCL5 and IL6 in A549 and 16HBE cells. Thus, Intelectin-1 is in the expression of inflammatory cytokines in the epithelial cells of the airway. Play an important role.
The second part is the role of ERK signaling pathway in intelectin-1 mediated expression of inflammatory cytokines CCL5 and IL6 in airway epithelial cells.
Objective: To investigate the mechanism of intelectin-1 involved in the expression of inflammatory cytokines CCL5 and IL-6 in airway epithelial cells.
Methods: IL-13 and PD98059 were used to group the human lung epithelial cell line A549 and 16HBE cell.PD98059 experiment group (1) control group, (2) IL-13 group and (3) IL-13+PD98059 group. Then RealTimePCR method was used to detect the mRNA expression of the cytokine CCL5 and IL6. After inhibiting the expression of intelectin-1 induced by IL-13 by RNA interference, the changes in the level of intelectin-1, ERK1/2 and P-ERK1/2 protein were detected by Western-Blot in the +humanITLN1shRNA plasmid group.
Results: after IL13 stimulated A549 and 16HBE cells with PD98059, the mRNA expression level of CCL5 and IL6 decreased significantly in IL13+PD98059 group than in IL13 group. P0.05. transfected to humanITLN1shRNA plasmid, intelectin-1 and protein expression level was higher than that of control group. Group -13 decreased, P0.05.
Conclusion: an inhibitor of ERK1/2, PD98059, can block the expression of CCL5 and IL6 in A549 and 16HBE cells induced by IL-13. Moreover, IL-13 stimulation increases ERK1/2 phosphorylation and intelectin-1 protein expression, but HumanITLLN1-shRNA plasmid transfection inhibits the expression of IL-13 induced proteins and phosphorylation. The ERK1/2 pathway can regulate the expression of IL-13 induced CCL5 and IL6, and the Intelectin-1 gene participates in the activation of ERK1/2 in A549 and 16HBE cells induced by IL-13, so we can think that the Intelectin-1 gene may be involved in IL-13 induced and expressed expressions by activating the ERK1/2 signaling pathway.
【學(xué)位授予單位】：華中科技大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2012
【分類號(hào)】：R562.25

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9 張敏,吳壯,徐軍;損傷氣道上皮組織轉(zhuǎn)化在氣道重塑中的作用[J];醫(yī)學(xué)研究生學(xué)報(bào);2004年11期

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