孟鲁斯特对哮喘模型IL-5mRNA和IL-5蛋白表达的影响

目的探讨白三烯受体拮抗剂孟鲁斯特(MK)对哮喘小鼠IL-5mRNA、IL-5蛋白表达的影响.方法采用原位杂交、免疫组化LSAB法,检测哮喘小鼠及孟鲁斯特治疗后哮喘小鼠骨髓细胞IL-5mRNA的表达及肺、骨髓、脾IL-5蛋白的表达情况.结果孟鲁斯特可显著减轻哮喘小鼠肺组织炎症细胞浸润、细支气管痉挛、粘液分泌等;亦可减少骨髓IL-5mRNA阳性细胞数(P＜0.02),并使骨髓、肺、脾IL-5蛋白表达下降.结论白三烯受体拮抗剂孟鲁斯特不仅使肺部炎症显著减轻,也抑制骨髓细胞表达IL-5mRNA、IL-5蛋白,提示白三烯可能通过调节炎症细胞、细胞因子合成来应答过敏原反应.     

孟鲁司特和地塞米松对哮喘炎症的作用

目的探讨孟鲁司特(MK)和地塞米松(Dex)对哮喘炎症的影响。方法建立哮喘动物模型,并分别给予MK和Dex治疗。检测肺泡灌洗液(BALF)和肺组织病理学改变;采用原位杂交法检测肺和骨髓细胞IL-5mRNA的表达;免疫组化法检测骨髓IL-5免疫反应阳性细胞;流式细胞仪检测骨髓CD34 和CD3 细胞。结果MK和Dex治疗组BALF细胞总数、嗜酸粒细胞数均较哮喘组减少(P<0.01),并且两治疗组比较也有显著性差异(P<0.05);病理结果显示,哮喘组肺组织气道痉挛、炎性细胞浸润明显,两治疗组肺组织炎症明显改善。MK组和Dex组肺组织和骨髓细胞IL-5mRNA表达显著低于哮喘组(P<0.05,P<0.01),两治疗组比较有显著性差异(P<0.05);两治疗组骨髓IL-5免疫反应细胞和CD34 、CD3 细胞亦较哮喘组显著减少(P<0.01,P<0.05),但两治疗组比较无统计学差异(P>0.05)。结论MK和Dex均可显著抑制气道炎症和肺、骨髓细胞表达IL-5 mRNA,尽管MK某些方面逊色于Dex,但提示皮质激素与白三烯受体拮抗剂的联合应用可能是治疗哮喘的新方向。     

孟鲁司特和地塞米松对哮喘炎症的作用

目的 探讨孟鲁司特(MK)和地塞米松(Dex)对哮喘炎症的影响.方法 建立哮喘动物模型,并分别给予MK和Dex治疗.检测肺泡灌洗液(BALF)和肺组织病理学改变;采用原位杂交法检测肺和骨髓细胞IL-5mRNA的表达;免疫组化法检测骨髓IL-5免疫反应阳性细胞;流式细胞仪检测骨髓CD34+和CD3+细胞.结果 MK和Dex治疗组BALF细胞总数、嗜酸粒细胞数均较哮喘组减少(P＜0.01),并且两治疗组比较也有显著性差异(P＜0.05);病理结果显示,哮喘组肺组织气道痉挛、炎性细胞浸润明显,两治疗组肺组织炎症明显改善.MK组和Dex组肺组织和骨髓细胞IL-5mRNA表达显著低于哮喘组(P＜0.05,P＜0.01),两治疗组比较有显著性差异(P＜0.05);两治疗组骨髓IL-5免疫反应细胞和CD34+、CD3+细胞亦较哮喘组显著减少(P＜0.01,P＜0.05),但两治疗组比较无统计学差异(P＞0.05).结论 MK和Dex均可显著抑制气道炎症和肺、骨髓细胞表达IL-5 mRNA,尽管MK某些方面逊色于Dex,但提示皮质激素与白三烯受体拮抗剂的联合应用可能是治疗哮喘的新方向.     

白三烯受体拮抗剂对哮喘小鼠肺组织IL-10表达的影响

目的检测白介素-10（IL-10）在哮喘小鼠肺组织中的表达及白三烯受体拮抗剂对其的影响。方法72只Balb/c小鼠随机分为哮喘组（A组）、孟鲁司特治疗组（B组）3组、生理盐水对照组（C组）,每组24只。各组均设1、2、3、4周4个时段。HE染色观察小鼠肺组织病理改变,免疫组化标记分析IL-10在肺组织的表达。结果HE染色B组肺组织炎症较A组明显减轻;A组、B组肺组织IL-10的表达在各时间段均显著低于C组（均P〈0.01）;B组肺组织IL-10的表达随治疗时间的延长显著增加,且与A组比较有显著差异（均P〈0.01）。结论白三烯受体拮抗剂治疗哮喘小鼠能抑制气道炎症而增加IL-10的生成,但白三烯受体拮抗剂和IL-10的关系有待进一步研究。     

白三烯拮抗剂顺尔宁对儿童哮喘的肺功能影响

哮喘是一种慢性气道炎症，半胱氨酰白三烯(CysLTS)作为重要的介质可致强烈的气道收缩和局部炎症，白三烯受体拮抗剂是哮喘防治的趋势。为了观察白三烯受体拮抗剂顺尔宁(孟鲁斯特钠)对哮喘儿童肺功能的影响，我们对哮喘患儿进行了服用该药前后的肺通气功能检测，现分析如下。     

孟鲁司特对哮喘肺组织白介素-5和白介素-13mRNA表达的影响

白三烯具有众多的生物学活性,其在哮喘发生、发展过程中的多个环节起作用。白三烯受体拮抗剂是近年发展起来的一类新型非类固醇类抗炎药物,众多的临床随机、双盲、对照和多中心研究表明,白三烯受体拮抗剂可明显改善轻一中度哮喘患者的肺功能和临床症状,提高生活质量,特别是对运动性哮喘、不耐受阿司匹林哮喘的作用更显著。本研究旨在探讨白三烯受体拮抗剂孟鲁司特(MK)对哮喘模型肺组织白介素(IL)-5和IL-13mRNA表达的影响及气道炎症的控制,为临床合理治疗哮喘提供依据。     

Th2细胞因子调节哮喘炎症细胞转运机制的研究

目的 探讨Th2细胞因子IL-5、IL-13调节哮喘炎症过程中肺和骨髓之间的细胞转运机制。方法 建立哮喘动物模型,获取肺泡灌洗液,检测IL-5、IFN-γ,浓度并进行病理分析;应用原位杂交技术检测肺组织IL-5、IL-13 mRNA表达和骨髓IL-5mRNA表达;免疫组化法观察肺、骨髓IL-5免疫反应细胞;流式细胞仪检测骨髓CD34、CD3阳性细胞。结果 哮喘组肺泡灌洗液IL-5浓度明显高于对照组(P<0.001);哮喘组肺组织病理改变显示小气道痉挛,管壁周围炎性细胞浸润,以嗜酸粒细胞、淋巴细胞为主;哮喘组肺组织IL-5、IL-13 mRNA表达较对照组显著增加(P<0.01);哮喘组骨髓IL-5 mRNA阳性细胞明显增加(P<0.001),与肺组织IL-5 mRNA表达的增高密切相关(P<0.05);此外,哮喘组肺组织和骨髓IL-5免疫反应细胞显著增加(P<0.01),骨髓CD34、CD3细胞均显著增高(P<0.01),并且CD34增高与骨髓细胞表达IL-5 mRNA密切相关(P<0.05)。结论IL-5可能在转录和转录后水平均参与调节骨髓嗜酸粒细胞的功能和炎症细胞在肺和骨髓之间的转运。     

白三烯受体拮抗剂孟鲁斯特对小鼠气道炎症的抑制作用

[目的]探讨白三烯受体1拮抗剂孟鲁斯特(montelukast,MK)抑制小鼠气道炎症的作用及可能的机制.[方法]致敏的BALB/c小鼠持续吸入10 g/L雾化卵白蛋白(OVA)30 min,OVA吸入前2 d开始连续3 d或5 d尾静脉给予MK或生理盐水(saline),OVA吸入后24 h及72 h取材,瑞氏染色观察支气管肺泡灌洗液(bronchoalveolarlavagefluid,BALF)中炎症细胞的渗出情况;ELISA方法检测血清、BALF和肺组织中有关细胞因子水平;HE、刚果红染色观察肺组织炎症细胞的渗出;免疫组化染色观察血管内皮细胞黏附分子-1(VCAM-1)和嗜酸性粒细胞趋化因子(eotaxin)的表达;原位杂交研究IL-5 mRNA的变化.[结果]给予MK 5 d减少BALF嗜酸性粒细胞渗出达90%以上,嗜酸性粒细胞减少随MK剂量(10、25、62.5 mg/kg)的增加呈量效关系.ELISA结果表明给予3 d MK使肺、血清和BALF中IL-5、IL-4水平显著降低,肺IL-13含量也明显减少(P＜0.05),但MK组肺组织eotaxan下降与saline组比较无明显差异(P＞0.05).免疫组化显示MK组肺组织VCAM-1和eotaxin表达比saline组明显减弱;原位杂交可见MK组肺组织IL-5 mRNA的表达比saline组减弱.[结论]MK减轻气道炎症,可能通过抑制VCAM-1表达和IL-5、IL-4、IL-13等细胞因子分泌起作用.急性哮喘中应用大剂量MK抗炎治疗值得进一步探讨.     

Th2细胞因子调节哮喘炎症细胞转运机制的研究

目的探讨Th2细胞因子IL-5、IL-13调节哮喘炎症过程中肺和骨髓之间的细胞转运机制.方法建立哮喘动物模型,获取肺泡灌洗液,检测IL-5、IFN-γ浓度并进行病理分析;应用原位杂交技术检测肺组织IL-5、IL-13 mRNA表达和骨髓IL-5mRNA表达;免疫组化法观察肺、骨髓IL-5免疫反应细胞;流式细胞仪检测骨髓CD34、CD3阳性细胞.结果哮喘组肺泡灌洗液IL-5浓度明显高于对照组(P＜0.001);哮喘组肺组织病理改变显示小气道痉挛,管壁周围炎性细胞浸润,以嗜酸粒细胞、淋巴细胞为主;哮喘组肺组织IL-5、IL-13 mRNA表达较对照组显著增加(P＜0.01);哮喘组骨髓IL-5 mRNA阳性细胞明显增加(P＜0.001),与肺组织IL-5 mRNA表达的增高密切相关(P＜0.05);此外,哮喘组肺组织和骨髓IL-5免疫反应细胞显著增加(P＜0.01),骨髓CD34、CD3细胞均显著增高(P＜0.01),并且CD34增高与骨髓细胞表达IL-5 mRNA密切相关(P＜0.05).结论IL-5可能在转录和转录后水平均参与调节骨髓嗜酸粒细胞的功能和炎症细胞在肺和骨髓之间的转运.     

白三烯受体拮抗剂对哮喘小鼠气道重塑及细胞周期蛋白D1的表达影响

目的：研究应用白三烯受体拈抗剂（孟鲁司特钠）对哮喘小鼠肺组织中细胞周期蛋白D1（Cyclin D1）的表达影响及对支气管哮喘气道重塑的作用，探讨白三烯受体拮抗剂在哮喘治疗中的作用。方法：将30只BALB／c小鼠随机分为正常对照组、哮喘组、孟鲁司特钠组3组，每组10只；卵蛋白致敏和激发建立哮喘小鼠模型；HE染色观察各组气道炎症发生及气道结构改变情况；免疫组化观察肺组织中Cyclin D1的表达及定位；RT-PCR及Western-blot测定各组小鼠肺组织中Cyclin D1的mRNA和蛋白表达变化。结果：HE染色提示哮喘组与对照组相比出现嗜酸性粒细胞浸润增多、纤毛脱失、平滑肌细胞层增厚等改变．而治疗组上述改变较哮喘组为轻；免疫组化显示Cyclin D1在哮喘小鼠气道平滑肌细胞、内皮细胞、成纤维细胞中皆有表达而在对照组中表达减弱（P〈0．05），而治疗组表达量较哮喘组低（P〈0．05）；RT-PCR及Western blot检测发现Cyclin D1在哮喘组表达较对照组为高（P〈0．01），而治疗组表达量低于哮喘组（P〈0．01）。结论：哮喘小鼠肺组织中Cyclin D1表达量较正常组为高；白三烯受体拮抗剂能够抑制Cyclin D1表达，减轻气道炎症反应、延缓气道重塑进程。     

Effects of glucocorticoid and cysteinyl leukotriene 1 receptor antagonist on CD34+ hematopoietic cells in bone marrow of asthmatic mice

Background Corticosteroids remain the most effective therapy available for asthma. They have widespread effects on asthmatic airway inflammation. However, little is known about the effects of corticosteroids on the production of bone marrow inflammatory cells in asthma. This study observed the effects of glucocorticoid and cysteinyl leukotriene 1 receptor antagonist on CD34+ hematopoietic cells, so as to explore the possible effectiveness of a bone marrow-targeted anti-inflammatory strategy. Methods Balb/c mice were sensitized and challenged with ovalbumin (OVA) to establish an asthmatic model. For two consecutive weeks, asthmatic mice were challenged with OVA while being given either prednisone, montelukast, prednisone plus montelukast, or sterile saline solution. The mice were killed 24 hours after the last challenge with OVA, and bronchoalveolar lavage fluid (BALF), peripheral blood, and bone marrow were collected. Eosinophils in peripheral blood and BALF, and nucleated cells in BALF, peripheral blood, and bone marrow were counted. The percentages of CD34+ cells, CD4+ T lymphocytes and CD8+ T lymphocytes among nucleated cells in peripheral blood and bone marrow were counted by flow cytometry. Immunocytochemistry and in situ hybridization were employed to detect expression of CD34 and interleukin (IL)-5Rα mRNA (CD34+ IL-5Rα mRNA+ cells) among bone marrow hematopoietic cells. Results Compared with the sterile saline solution group, the number of eosinophils in BALF and peripheral blood, CD34+ cells in peripheral blood and bone marrow, and CD34+ IL-5Rα mRNA+ cells in bone marrow of mice from the prednisone and prednisone plus montelukast groups were significantly lower （P&lt;0.01）. The number of eosinophils in BALF from the montelukast group was also significantly lower （P&lt;0.05）. Conclusions The results suggest that, in this asthmatic mouse model, prednisone probably inhibits proliferation, differentiation, and migration of CD34+ cells in bone marrow, blocks eosinophilopoiesis in bone marrow, and interferes with eosinophil migration into peripheral blood and subsequent recruitment in the airway. In addition, montelukast may suppress eosinophil infiltration into the lungs of asthmatic mice. However, a significant inhibitory effect of montelukast on the proliferation and migration of CD34+ cells and a cooperating effect with prednisone on bone marrow of asthmatic mice were not observed.     

Effect of NK cells on GVHD in H-2 haploidentical bone marrow transplantation in mice

Objective To study the effect of natural killer (NK) cells on graft-versus-host disease (GVHD) after H-2 haploidentical bone marrow transplantation (BMT) in mice. Methods Murine model of H-2 haploidentical BMT was established by using Balb/c (H-2d) mouse as recipient, and Balb/c(H-2d)×C57BL/6 (H-2b) (H-2d/b) mouse as donor. Lethally irradiated Balb/c (H-2d) mice were transplanted with the bone marrow cells from Balb/c(H-2d)×C57BL/6(H-2b) (H-2d/b) mice containing donor spleen cells and/or NK cells. GVHD and survival rates were studied by observation of clinical manifestations and pathological changes. ResultsIn the group of bone marrow spleen cells, GVHD was induced in 90% mice; but in the group plus with low amount of NK cells,GVHD was induced in 20% mice; and in the group transplanted with high amount of NK cells, GVHD was induced only in 10% mice. Compared to the group transplanted only with BM plus spleen cells, the incidences of GVHD in the latter two groups decreased significantly (P＜0.01) and the survival rates at different periods of 15, 30, 45 and 60 days increased obviously (P＜0.01 ). Conclusion In mouse H-2 haploidentical BMT, alloreactive NK cells can reduce the incidence of GVHD and increase the survival rate.     

吉西他滨对小鼠实验性自身免疫性心肌炎的影响

目的: 研究吉西他滨对实验性自身免疫性心肌炎(experimental autoimmune myocarditis,EAM)模型小鼠的治疗作用。方法: 取15只Balb／c小鼠构建EAM模型,分为对照组,EAM组,EAM+吉西他滨组,每组5只;在第21天,取眼球血,颈椎脱臼处死小鼠,取心脏组织行HE染色,光镜下观察淋巴细胞浸润情况,并行炎症评分;流式细胞术检测脾脏组织中骨髓来源的抑制性细胞(myeloid derived suppressor cell,MDSC)和Th17细胞比例;ELISA法检测血清中IL 17A浓度;qRT PCR检测心脏组织中IL 17A mRNA含量。取正常Balb／c小鼠脾脏分选MDSC和Nave CD4+T细胞,分为活化组,诱导组,共培养组,流式细胞术检测各组Th17比例。结果： 与对照组比较,EAM组心肌组织以炎性细胞浸润和心肌细胞坏死为主,组织炎症评分明显增高(P<0.05);与EAM组比较,EAM+吉西他滨组炎性细胞的浸润和心肌细胞坏死减少,组织炎症评分明显降低(P<0.05);与对照组比较,EAM组脾脏中MDSC和Th17比例明显增加(P<0.05);与EAM组比较,EAM+吉西他滨组二者比例明显降低(P<0.05)。与对照组相比,EAM组IL 17A浓度和IL 17A mRNA表达明显增高(P<0.05);与EAM组比较,EAM+吉西他滨组二者含量明显降低(P<0.05)。与诱导组比较,共培养组Th17比例明显增加(P<0.05)。 结论： 吉西他滨可能通过降低EAM模型小鼠脾脏中MDSC数量,进而抑制NaveCD4+T细胞向Th17细胞的分化从而缓解心肌炎症。     

日本血吸虫感染小鼠脾细胞体外IL-2转录水平的实验观察

应用RT PCR方法对日本血吸虫感染小鼠脾细胞体外在SEA与ConA诱导下产生的IL 2从mRNA转录水平进行研究 ,以探讨该细胞因子mRNA转录水平的动态变化及其在肉芽肿形成与调节过程中的作用。结果显示 ,未感染和感染 3周小鼠脾细胞均无IL 2表达 ,感染后第 5周的小鼠脾细胞出现IL 2特异性条带 ,感染后第 8周IL 2表达明显增强 ,感染后第 1 0、1 2周无论SEA或ConA都不能诱导IL 2mRNA的转录。表明IL 2表达的动态变化与肉芽肿的形成、发展及调节相平行 ,提示IL 2可能在肉芽肿形成和调节过程中起重要作用。     

间充质干细胞联合NK细胞输注抑制DC减轻aGVHD

【目的】 观察骨髓MSC联合NK细胞输注对小鼠异基因骨髓移植后aGVHD的影响,初步探讨其作用机制?【方法】 分离C57BL/6小鼠骨髓细胞,体外培养MSC;取C57BL/6小鼠脾脏细胞,磁珠分选NK细胞;建立C57BL/6→BALB/c小鼠异基因骨髓移植模型,接受移植小鼠随机分为4组,每组10只小鼠,MSC和NK细胞移植组,MSC移植组,NK细胞移植组和培养基对照组?根据aGVHD分值,肝?脾?小肠aGVHD病理损害和平均存活时间,评价aGVHD的程度?ELISA法检测小鼠血清中IFNγ和IL-12的含量?流式细胞术检测受鼠脾脏细胞CD11c和CD86的表达情况?【结果】 根据GVHD分值,肝?脾?小肠aGVHD病理损害和平均存活时间综合评价,与培养基对照组比较,MSC联合NK细胞移植组,MSC移植组和NK细胞移植组,发生aGVHD的程度均减轻,以MSC联合NK细胞移植组减轻最为明显?IFNγ的含量,NK细胞组明显高于MSC联合NK细胞移植组,MSC移植组和培养基对照组?IL-12的含量,MSC联合NK细胞移植组低于NK细胞移植组和培养基对照组,MSC移植组低于培养基对照组?脾脏DC细胞的含量,MSC联合NK细胞移植组未成熟DC(CD11c+CD86-)和成熟DC(CD11c+CD86+)均低于MSC移植组,NK细胞组和培养基对照组?【结论】 MSC联合NK细胞输注降低DC细胞数量,减轻aGVHD,延长小鼠生存时间?     

哮喘气道炎症中嗜酸性粒细胞凋亡与 IL-5、IL-10关系的研究

目的　动态观察哮喘动物模型气道嗜酸性细胞凋亡在炎症中的意义和调控机理，研究IL-5和IL-10对凋亡的调节作用。方法　卵白蛋白（OVA）腹腔注射与雾化吸入诱发BALB/c小鼠哮喘发作。在激发后0、8、24、48、96小时及7、14天行BAL，ELISA法测定IL-5、IL-10浓度。CD15、CD49d双色标记嗜酸细胞(EOS)，流式细胞仪上检测EOS凋亡率。结果　OVA激发后电镜观察显示肺内有明显炎性细胞浸润和细胞凋亡。哮喘组EOS凋亡总体水平与对照大体相似。EOS凋亡率与IL-10/IL-5比值密切相关。结论　IL-5和IL-10分别上行和下行调节哮喘气道炎症。气道局部有EOS凋亡现象，并受到IL-5、IL-10相互作用的调节。     

Relationship between bone marrow-derived CD34+ cells expressing interleukin-5 receptor messenger RNA and asthmatic airway inflammation

Background Asthma is clinically related with the degree of eosinophilic inflammation.How asthmatic airway inflammation is affected is still poorly understood. So the effects of bone marrow-derived hematopoietic cells expressing CD34 (CD34+) and interleukin-5 (IL-5) receptor messenger RNA (IL-5R mRNA+) on asthmatic airway inflammation were investigated.Methods Balb/c mice were sensitized and challenged by ovalbumin (OVA) to establish an asthmatic model while control mice were sensitized and exposed to sterile saline. The mice were killed at different time points after being challenged by OVA and sterile saline. Then, bronchoalveolar lavage fluid (BALF), peripheral blood (PB) and bone marrow (BM) were prepared. Eosinophils in PB (PBEOS) and BALF (BALFEOS), nuclear cells in BALF, PB and BM were counted. By flow cytometry, the percentage of CD34+ cells to nucleated cells in PB, BM and the relative number of CD34+ cells in PB (PBCD34+) and BM (BMCD34+) were calculated. Immunocytochemistry and in situ hybridization were used to investigate the hematopoietic cells with co-localized expression of CD34 and IL-5R mRNA in BM (BMCD34+IL-5R mRNA+). The percentage of BMCD34+IL-5R mRNA+ to BMCD34+ was calculated. Results Twelve hours after challenge by OVA, BALFEOS and PBEOS in the experimental group were significantly higher than those in the control group （P&lt;0.01). Twenty-four hours after OVA challenge, BALFEOS, PBEOS and BMCD34+IL-5R mRNA+ were elevated maximally, significantly different from those in the control group （P&lt;0.01). Forty-eight hours after OVA challenge, BALFEOS and BMCD34+IL-5R mRNA+ were still significantly higher than those of the controls （P&lt;0.01). The other markers reverted to normal. In 60 mice, BMCD34+IL-5R mRNA+ was closely correlated with the BALEOS, PBEOS, BMCD34+ and BMCD34+ （%) （P&lt;0.05).Conclusions The amount of CD34+ cells expressing IL-5R mRNA increased in the BM of asthmatic model mice, which favors eosinophilopoiesis and eosinophilic airway inflammation. A signal pathway exists between the lungs and the bone marrow, which is involved in the initiation and maintenance of asthmatic airway inflammation.     

耐受性树突状细胞对哮喘小鼠气道变应性炎症反应的抑制作用

目的: 用卵白蛋白(OVA)刺激的未成熟树突状细胞(immature dendritic cell, imDC)免疫小鼠,观察其对小鼠OVA激发的气道过敏性炎症反应的抑制作用,探讨耐受性树突状细胞疫苗诱导免疫耐受的可能机制,为临床防治哮喘提供新的思路.方法: 制备BALB/c小鼠髓性imDC.其余BALB/c小鼠分4组,10只/组:其中两组于第-7天分别注射无菌PBS(PBS组)、OVA刺激的imDC(imDC组),第三组于第13～20天注射地塞米松(地塞米松组),第四组不作任何处理(健康对照组);除健康对照组外,其余各组诱导哮喘反应:第0天和第9天分别注射OVA致敏,14～20天每日予OVA气雾攻击.第21天每组处理5只小鼠,检测肺部炎症细胞浸润及嗜酸性粒细胞比例、气道黏液分泌、脾细胞Th1/Th2型细胞因子表达及脾细胞中CD4 CD25 细胞比例;第49天,处理剩余动物,观察哮喘预后.结果: mDC注射组肺部炎症浸润较轻,脾细胞表达白细胞介素(IL)-13、4降低而γ-干扰素(IFN-γ)无显著影响,脾细胞中CD4 CD25 细胞比例较高,气道黏液分泌则少于PBS组,且预后良好. 结论: 过敏原特异性imDC疫苗注射可在一定程度上缓解哮喘小鼠气道的变应性炎症反应.     

联合应用IL-2和IL-3的基因疗法增强骨髓移植后骨髓细胞毒活性及抗肿瘤效果的实验研究

目的：探讨联合应用成纤维细胞介导ＩＬ２和ＩＬ３的基因疗法对骨髓移植（ＢＭＴ）后荷瘤小鼠抗肿瘤作用的效果及机理。方法：将分别转染ＩＬ２基因及ＩＬ３基因的ＮＩＨ３Ｔ３细胞以单独或联合方式移植至ＢＭＴ的荷瘤小鼠腹腔内８ｄ后，取出小鼠骨髓细胞检测杀伤活性的变化以及ＩＬ２受体的表达，并观察荷瘤小鼠的存活期。结果：ＩＬ３基因治疗虽然可加速ＢＭＴ后造血重建过程，但对骨髓细胞的ＮＫ、ＬＡＫ活性具有一定的抑制作用；ＩＬ２基因治疗可明显提高骨髓细胞的杀伤活性；联合应用基因治疗后荷瘤小鼠骨髓ＮＫ、ＬＡＫ活性及骨髓细胞ＣＤ２５表达升高，明显延长大剂量化疗后接受ＢＭＴ的荷瘤小鼠的存活期。结论：联合应用ＩＬ２和ＩＬ３的基因疗法能协同提高骨髓细胞ＩＬ２受体表达水平，提高骨髓细胞毒活性，增强ＢＭＴ后的抗肿瘤效果。