哮喘患者淋巴细胞粒细胞—巨噬细胞集落刺激因子mRNA的表达

哮喘患者淋巴细胞粒细胞－巨噬细胞集落刺激因子ｍＲＮＡ的表达金远林王长征王春霞钱桂生活化的Ｔ淋巴细胞产生的细胞因子白细胞介素（ＩＬ）－５、粒细胞－巨噬细胞集落刺激因子（ＧＭ－ＣＳＦ）及ＩＬ－３，在以嗜酸细胞（Ｅｏｓ）为主的哮喘非特异性气道炎症产生中起重...     

哮喘豚鼠肺组织粒细胞-巨噬细胞集落刺激因子mRNA表达及雷公藤的影响

目的探讨粒细胞－巨噬细胞集落刺激因子（ＧＭ－ＣＳＦ）在哮喘嗜酸细胞（Ｅｏｓ）炎症中的作用。方法建立哮喘豚鼠实验模型，用雷公藤处理，观察肺组织Ｅｏｓ密度，斑点分子杂交检测支气管肺组织ＧＭ－ＣＳＦｍＲＮＡ含量。结果哮喘组肺组织Ｅｏｓ浸润密度增加，ＧＭ－ＣＳＦｍＲＮＡ表达水平增高，与对照组相比差异有显著性（Ｐ＜０．０５）。雷公藤处理后ｍＲＮＡ表达显著降低，但Ｅｏｓ浸润密度减少不明显。结论ＧＭ－ＣＳＦｍＲＮＡ表达增加可能是导致哮喘Ｅｏｓ气道炎症的原因。雷公藤能抑制ＧＭ－ＣＳＦｍＲＮＡ表达，可能具有哮喘抗炎治疗的潜在应用价值。     

支气管哮喘患者粒—基噬细胞集落刺激因子mRNA表达的研究

目的 探讨利用无创伤性方法寻找较为特异性地反映哮喘患气道炎症的客观指标。方法 通过研究哮喘患气道粘膜细胞粒－巨噬细胞集落刺激因子（ＧＭ－ＣＳＦ）ｍＲＮＡ表达,并以此为参照,分析哮喘患诱导痰细胞ＧＭ－ＣＳＦ ｍＲＮＡ变化,利用免疫组化结合逆转录聚合酶链反应（ＲＴ－ＰＣＲ）技术,分析哮喘组（１０例）气道粘膜细胞ＧＭ－ＣＳＦ ｍＲＮＡ的表达;用３％高渗盐水诱导痰液,利用ＲＴ－ＰＣＲ技术分析哮喘组（     

粒细胞—巨噬细胞集落刺激因子对人气道平滑肌细胞内皮素…

目的 观察炎前细胞因子粒细胞－巨噬细胞集落刺激因子（ＧＭ－ＣＳＦ）对培养的人气道平滑肌细胞内皮素－１（ＥＴ－１）基因及内皮素转换酶（ＥＣＥ）基因表达的影响及茶碱对此种表达的作用，探讨在炎症环境下气道平滑肌细胞在气道高反应性发生，发展中的作用及低剂量茶碱在遏制气道高反应性的可能机制。方法 分别以ＧＭ－ＣＳＦ（１０００μｇ／ｍｌ）或与茶碱（１２５ｎｇ／ｍｌ）联合刺激离体培养人气道平滑肌细胞８小时，运用     

粒细胞——巨噬细胞集落刺激因子的研究现状及临床应用

集落刺激因子(Colony Stimulating Factors)是一组控制粒细胞、单核一巨噬细胞和某些有关的造血细胞增殖和分化的糖蛋白,根据不同的分化阶段和造血祖细胞,分为粒细胞一巨噬细胞集落刺激因子(GM—CSF)、粒细胞集落刺激因子(G—CSF)、巨噬细胞集落刺激因子(M—CSF)以及多潜能集落刺激因子(Multi—CSF)又称白细胞介素—3(IL—3)。现就近年来GM—CSF研究进展及临床应用综述如下。     

哮喘豚鼠肺组织中嗜酸细胞凋亡与白细胞介素5mRNA表达？…

目的 探讨哮喘时嗜酸细胞（ＥＯＳ）凋亡与肺组织白细胞介素５（ＩＬ－５）ｍＲＮＡ表达的关系。方法 将豚鼠随机分为对照组（正常组７只）、哮喘组（８只）、地塞米松组（８只），应用脱氧核糖核酸末端转移酶介导的缺口末端标记（ＴＵＮＥＬ）技术和原位杂交方法，检测支气管肺泡灌洗液（ＢＡＬＦ）中不同密度ＥＯＳ凋亡百分比和肺组织ＩＬ－５ｍＲＮＡ的表达。结果 （１）正常对照组ＢＡＬＦ中低密度ＥＯＳ、正常密度ＥＯＳ凋是     

哮喘豚鼠肺组织白细胞介素5 mRNA表达等研究

采用卵蛋白（ＯＡ）吸入诱发豚鼠哮喘模型，分析支气管肺泡灌洗液嗜酸性粒细胞（ＥＯＳ）细胞数目改变，检测不同密度ＥＯＳ数目及比例改变，并采用原位杂交技术检测肺组织白细胞介素５（ＩＬ５）ｍＲＮＡ表达，以及地塞米松对其表达的影响。方法３６只豚鼠雌雄不限，体...     

Granulocyte-macrophage colony-stimulating factor mRNA stabilization enhances transgenic expression in normal cells and tissues

To increase transgenic production of granulocyte-macrophage colony- stimulating factor (GM-CSF), we mutated the mRNA's 3'-untranslated region, AUUUA instability elements. Expression vectors containing human or murine GM-CSF cDNAs coding for wild-type (GM-AUUUA) or mutant versions with reiterated AUGUA repeats (GM-AUGUA) were transfected into cells in culture or animals using particle-mediated gene-transfer technology. Normal peripheral blood mononuclear cells accumulated 20- fold greater levels of GM-CSF mRNA and secreted comparably greater amounts of cytokine after transfection with hGM-AUGUA expression vectors versus hGM-AUUUA. hGM-AUGUA mRNA was fivefold more stable (t 1/2 = 95 minutes) than hGM-AUUUA mRNA (t 1/2 = 20 minutes), accounting for elevated steady-state levels. Transfection site extracts and serum samples obtained 24 hours after gene transfer of hGM-AUGUA cDNA into mouse skin contained greater than 32 ng/mL and 650 pg/mL of GM-CSF protein, respectively, compared with 0.33 ng/mL and less than 8 pg/mL for hGM-AUUUA cDNA. GM-CSF produced from mGM-AUGUA cDNA transfected into rat abdominal epidermis induced a profound neutrophil infiltrate. These data suggest a novel strategy for enhanced production of biologically active cytokines by normal cells after in vivo gene transfer.     

细胞间粘附分子1mRNA在哮喘豚鼠支气管组织中的原位表达

为了解哮喘豚鼠支气管组织中的细胞间粘附分子１（ＩＣＡＭ－１）ｍＲＮＡ表达情况，将实验豚鼠随机分为正常对照组、氟美松组和哮喘组，采用原位杂交方法显示ＩＣＡＭ－１ｍＲＮＡ的表达变化，用ＨＥ染色方法来测定炎细胞在支气管粘膜中的浸润程度。原位杂交结果显示，ＩＣＡＭ－１ｍＲＮＡ主要在支气管粘膜下的小血管、毛细血管内皮细胞以及支气管上皮细胞的胞浆内表达。定量分析结果表明，哮喘组豚鼠支气管组织表达ＩＣＡＭ－１ｍＲＮＡ较正常对照组及氟美松组显著增加（Ｐ＜０．０２，Ｐ＜０．０５），哮喘豚鼠支气管组织ＩＣＡＭ－１ｍＲＮＡ的表达量与炎细胞总数之间显著相关（Ｐ＜０．０５）。提示支气管粘膜组织ＩＣＡＭ－１ｍＲＮＡ表达与哮喘支气管粘膜嗜酸细胞为主的炎细胞浸润有关，糖皮质激素能够抑制细胞粘附分子的表达。     

In vivo effect of human granulocyte-macrophage colony-stimulating factor on megakaryocytopoiesis.

The effect of granulocyte-macrophage colony-stimulating factor (GM-CSF) on megakaryocytopoiesis and platelet production was investigated in patients with normal hematopoiesis. Three findings indicated that GM-CSF plays a role in megakaryocytopoiesis. During treatment with GM-CSF (recombinant mammalian, glycosylated; Sandoz/Schering-Plough, 5.5 micrograms protein/kg/d, subcutaneously for 3 days) the percentage of megakaryocyte progenitors (megakaryocyte colony forming unit [CFU-Mk]) in S phase (evaluated by the suicide technique with high 3H-Tdr doses) increased from 31% +/- 16% to 88% +/- 11%; and the maturation profile of megakaryocytes was modified, with a relative increase in more immature stage I-III forms. Moreover, by autoradiography (after incubation of marrow cells with 125I-labeled GM-CSF) specific GM-CSF receptors were detectable on megakaryocytes. Nevertheless, the proliferative stimulus induced on the progenitors was not accompanied by enhanced platelet production (by contrast with the marked granulomonocytosis). It may be suggested that other cytokines are involved in the regulation of the intermediate and terminal stages of megakaryocytopoiesis in vivo and that their intervention is an essential prerequisite to turn the GM-CSF-induced proliferative stimulus into enhanced platelet production.     

Uses of granulocyte-macrophage colony-stimulating factor in vaccine development

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a potent cytokine capable of inducing differentiation, proliferation, and activation of a variety of immunologically active cell populations. In addition to its effects on stimulating granulocytic hematopoiesis, it also facilitates development of both humoral and cellular mediated immunity. Accordingly, strategies involving the use of GM-CSF as a vaccine adjuvant have attracted considerable attention. These strategies include the systemic administration of soluble GM-CSF with an immunogen, and also its use as part of gene therapy approaches to immunization. Because of the potency of this cytokine as an immune adjuvant, particular interest has focused on its use to overcome poorly immunogenic antigens such as those associated with intracellular infections and cancer. This review focuses on recent advances in the use of GM-CSF as a vaccine adjuvant.