心肌疾病患儿粒细胞-巨噬细胞集落刺激因子与抗β-受体抗体的关系及其意义

目的探讨病毒性心肌炎(VMC)和扩张型心肌病(DCM)患儿粒细胞-巨噬细胞集落刺激因子(GM-CSF)与抗β-肾上腺素受体(简称β-受体)抗体的关系及其意义.方法采用放射免疫和免疫印转技术检测了30例VMC、14例DCM患儿GM-CSF和抗β-受体抗体.并与对照组25例健康儿对比.结果VMC和DCM患儿GM-CSF和抗β-受体抗体的阳性率分别为54.5%和79.55%,而25例健康儿分别为8%和0(P均<0.01);且GM-CSF与抗β-受体抗体的血浆水平呈正相关(r=0.4423,P<0.05).结论GM-CSF和抗β-受体抗体均参与了VMC和DCM患儿的发病,与β-受体功能异常、心肌自身免疫损伤有关.     

心肌疾病抗ADP／ATP载体抗体与粒细胞巨噬细胞集落刺激因子的？…

探讨病毒性心肌炎和扩张型心肌病的自身免疫发病机制。方法 采用免疫印转和放射免疫技术邮３０例ＶＭＣ，１４例ＤＣＭ患儿血浆中心肌线粒体ＡＤＰ／ＡＴ运载蛋白抗体和粒细胞－巨噬细胞集落刺激因子。结果 ＶＭＣ与ＤＣＭ患儿抗ＡＮＴ抗体和ＧＭ－ＣＳＦ的阳性率分别为７３％和５７％，而２５例正常健康儿分别为０和１２％，且抗ＡＮＴ抗血与ＧＭ－ＣＳＦ的血浆水平呈正相关。     

粒细胞巨噬细胞集落刺激因子与感染

粒细胞巨噬细胞集落刺激因子(GMCSF)是造血细胞因子家族中的成员,是一种能在造血干细胞、祖细胞和成熟细胞不同水平上促其生成的多向性造血因子和内源性调节因子。GMCSF作为一种内源性调节因子在抗感染免疫中对某些细菌、真菌、病毒和寄生虫感染中有重要作用。具有潜在的临床应用价值     

粒细胞-巨噬细胞集落刺激因子的研究进展

粒细胞一巨噬细胞集落刺激因子（GM—CSF）主要由体内激活的T细胞、单核巨噬细胞等产生。近年研究发现它是一种有广泛免疫活性的效应因子,在激活免疫反应中起重要作用,参与特异性抗体的产生。GM—CSF主要促进粒、巨噬细胞增殖、分化及功能成熟,提高宿主的防御能力,而且可以活化巨噬细胞产生依赖性细胞介导的细胞毒效应（ADCC）和多形性中性粒细胞（PMN）产生补体介导的吞噬作用,以及增强PMN的各种功能。GM—CSF还能提高C3bi及Fcr受体的表达,现就其近年来的研究进展作一综述。     

粒细胞、粒巨噬细胞集落刺激因子在新生儿期的应用

新生儿感染的发病率及病死率较高，吞噬细胞系统不成熟是主要原因这一，粒细胞，粒巨噬细胞集落刺激因子可刺激粒子巨噬细胞增殖，分化、增强中性粒细胞和单核巨噬细胞功能，临床上应用重组人类集落刺激因子治疗和预防新生儿感染取得了令人鼓舞的效果。     

粒细胞、粒巨噬细胞集落刺激因子在新生儿期的应用

新生儿感染的发病率及病死率较高，吞噬细胞系统不成熟是主要原因之一。粒细胞、粒巨噬细胞集落刺激因子可刺激粒巨噬细胞增殖、分化，增强中性粒细胞和单核巨噬细胞功能。临床上应用重组人类集落刺激因子治疗和预防新生儿感染取得了令人鼓舞的效果。     

粒细胞-巨噬细胞集落刺激因子联合乙肝疫苗对宫内感染HBV携带儿童治疗机制初探

目的从细胞因子水平初步探讨粒细胞一巨噬细胞集落刺激因子(GM—CSF)联合乙肝疫苗对宫内HBV感染携带儿童的疗效机制。方法采用ELISA和半定量逆转录-聚合酶链反应(RT—PCR)，对12例GM—CSF联合乙肝疫苗治疗后儿童、6例乙肝免疫球蛋白(HBIG)联合乙肝疫苗治疗后儿童及9例未治疗的宫内感染儿童外周血单个核细胞在PHA LPS、HBsAg及无刺激物时γ-干扰素、白细胞介素(IL)-4分泌及mRNA表达水平进行检测。结果与对照组比较，GM-CSF联合乙肝疫苗治疗儿童γ-干扰素自发分泌显著增加(P=0．017)，HBIG联合乙肝疫苗治疗儿童IL-4 mRNA转录显著降低(P=0．002)。结论GM—CSF联合乙肝疫苗治疗宫内感染HBV慢性携带儿童时HBV受抑制可能与γ-干扰素产生增多有关，HBIG联合乙肝疫苗治疗时IL-4转录受抑不影响HBV复制，提示慢性HBV感染治疗应以增强Th1应答为主。     

重组人粒-巨噬细胞集落刺激因子治疗儿童药物性粒细胞缺乏症18例

重组人粒 巨噬细胞集落刺激因子 (ｒＨｕＧＭ ＧＳＦ)能特异性刺激粒细胞和巨噬细胞的分化、增殖和成熟 ,并能提高效应细胞的免疫活性 ,起到加强机体免疫力和对抗感染的作用。骨髓抑制是抗癌药物的主要副作用 ,是化学治疗 (简称化疗 )中最显著的障碍因素 ,在临床上表现为粒细胞减少以及与之相关的感染。目前临床已将ｒＨｕＧＭ ＣＳＦ广泛用于强烈化疗及骨髓移植所致的白细胞减少症或粒细胞缺乏症。我们于 2 0 0 0年 3～ 6月将厦门特宝生物工程有限公司研制的ｒＨｕＧＭ ＣＳＦ(商品名 :特尔立 )用于化疗后药物性粒细胞减少症的治疗。对象和…     

新生儿肺炎血清粒细胞集落刺激因子的研究

粒细胞集落刺激因子（G－CSF）是一种体内产生的糖蛋白生长因子。在人体被细胞感染后明显升高。我们观察36例肺炎新生儿血清G－CSF水平。观察结果表明新生儿肺炎血清G－CSF升高，与对照组比较有非常显著差异（P＜0．001）。G－CSF阳性表明体内有细菌感染存在。临床上我们根据G－CSF水平酌情合理使用抗生素，并取得较好效果，因此我们认为血清G-GSF的检测对新生儿感染性疾病的抗生素应用有指导意义。     

急性白血病患儿应用重组粒细胞集落刺激因子诱导自身抗体产生及临床意义

目的　研究急性白血病患儿应用重组粒细胞集落刺激因子 (rhG CSF)后自身抗体的产生及其临床意义。方法　应用ELISA技术检测 10 4例正常儿童和 4 6例急性白血病患儿血清rhG CSF抗体。结果　共有 11例患儿在应用rhG CSF后检测到自身抗体 ,并均在 3个月内转阴。在抗体阴性和阳性组之间 ,rhG CFS疗程结束时的中性粒细胞数差异显著 (P <0 0 5 ) ,但与rhG CSF用量和病程无关。结论　应用rhG CSF诱导产生的自身抗体可抑制该制剂的生物学功能 ,监测抗体可预测rhG CSF对中性粒细胞的恢复效用。     

Protective effects of recombinant human granulocyte colony stimulating factor in a rat model of necrotizing enterocolitis

The role of cytokines and growth factors in the pathophysiology of neonatal necrotizing enterocolitis (NEC) is not defined clearly yet. The aim of this study was to determine the effects of recombinant human granulocyte colony stimulating factor (G-CSF) on intestinal cells in hypoxia-induced experimental NEC in rats. The study was experimented on Sprague Dawley rat pups. Group 1 (untreated, n = 7) rats were subjected to hypoxia–reoxygenation (H/O) and then were returned to standard conditions. Group 2 (G-CSF treated, n = 7) rats were subjected to H/O, and then were treated with G-CSF (100 μg/kg enterally) for 5 days. Group 3 was served as nonhypoxic controls. All animals were killed on day five, and histological examination was performed on intestinal samples. There were no histopathological changes in the control group. The histological findings in untreated rats were similar to those seen in neonatal NEC, with destruction of villi and crypts with extension to the muscularis layer. Intestinal damage was mild in group 2 and these histological changes were better than group 1, and worse than group 3. The mean of histologic grade of group 1 was 2.4 (range 2–3), and in the group 2, it was 1.2 (range 0–2). A difference was found when two groups were compared with each other (P < 0.05). In an experimental model of NEC, G-CSF could have a protective effect on intestinal damage.     

Serum concentration of granulocyte colony stimulating factor in term and preterm infants

We measured serum granulocyte colony stimulating factor (GCSF) concentration and absolute neutrophil count in four groups of infants: (1) 15 healthy term newborn infants; (2) 21 healthy preterm newborn infants, with mean (SD) birth weight 1583 (533) g, and gestational age 32.0 (3.8) weeks; (3) 5 infected newborn infants; (4) 22 6-month-old control infants. Median (range) serum GCSF concentration was 132.2 (41.5–176.0) pg/ml in term infants, 51.5 (1.8–175.7) pg/ml in preterm infants and 138.9 (54.1–449.8) pg/ml in 6-month-old control infants, with a significant reduction in preterm infants, as compared to term and control infants. GCSF levels were significantly higher in the infected infants, as compared to healthy neonates. Conclusion A significant positive relationship was found in term and preterm infants between serum GCSF concentration and gestational age or birth weight. No relationship was found between serum GCSF concen tration and neutrophil count. The low GCSF baseline levels may contribute to the increased incidence and severity of infection in preterm infants. Received: 17 May 1996 and in revised form: 20 July 1996 / Accepted: 29 July 1996     

Use of recombinant human granulocytemacrophage colony stimulating factor in an infant with reticular dysgenesis

We present the case of a 2-month-old infant with reticular dysgenesis who was treated with recombinant granulocyte-macrophage colony stimulating factor with the aim of stimulating granulopoiesis while awaiting bone marrow transplant.     

转粒细胞-巨噬细胞集落刺激因子基因真核表达质粒的构建及生物学活性鉴定

目的　构建小鼠转粒细胞 巨噬细胞集落刺激因子 (mGM CSF)真核表达质粒 pcDNA3 GM CSF ,转染红白血病细胞系FBL 3,并鉴定其活性。方法　采用分子克隆技术 ,构建mGM CSF真核表达质粒 pcDNA3 GM CSF ,电穿孔法将其导入红白血病细胞系FBL 3,G4 18筛选G4 18抗性细胞 ,限制性稀释法筛选G4 18抗性细胞克隆。PCR和RT PCR方法鉴定GM CSF基因整合和稳定表达。骨髓造血祖细胞增殖实验和骨髓造血祖细胞集落刺激实验鉴定其生物学活性。结果　采用PCR方法扩增mGM CSFcDNA序列 ,BamHⅠ和EcoRⅠ双酶切后装入 pcDNA3质粒 ,构建真核表达质粒 pcDNA3 GM CSF ,酶切和测序结果与预期相符 ,无插入、丢失、突变 ,方向正确。PCR和RT PCR结果显示 ,GM CSF基因整合到受体细胞染色体中并稳定表达。表达GM CSF的FBL 3 GM CSF细胞培养上清可明显刺激小鼠骨髓单个核细胞增殖 ,并能刺激干细胞形成克隆 ,形成克隆数为 (5 4 .6 7± 4 .83)个 ,形成率为 0 .5 4 7%。结论　构建mGM CSF真核表达质粒pcDNA3 GM CSF ,获得稳定表达该基因并具有生物学活性的细胞克隆 ,为制备转GM CSF基因瘤苗 ,探索白血病免疫治疗的可行性奠定基础     

转粒细胞-巨噬细胞集落刺激因子基因真核表达质粒的构建及生物活性鉴定

目的　构建小鼠转粒细胞 巨噬细胞集落刺激因子 (mGM CSF)真核表达质粒 pcDNA3 GM CSF ,转染红白血病细胞系FBL 3,并鉴定其活性。方法　采用分子克隆技术 ,构建mGM CSF真核表达质粒 pcDNA3 GM CSF ,电穿孔法将其导入红白血病细胞系FBL 3,G4 18筛选G4 18抗性细胞 ,限制性稀释法筛选G4 18抗性细胞克隆。PCR和RT PCR方法鉴定GM CSF基因整合和稳定表达。骨髓造血祖细胞增殖实验和骨髓造血祖细胞集落刺激实验鉴定其生物学活性。结果　采用PCR方法扩增mGM CSFcDNA序列 ,BamHⅠ和EcoRⅠ双酶切后装入 pcDNA3质粒 ,构建真核表达质粒 pcDNA3 GM CSF ,酶切和测序结果与预期相符 ,无插入、丢失、突变 ,方向正确。PCR和RT PCR结果显示 ,GM CSF基因整合到受体细胞染色体中并稳定表达。表达GM CSF的FBL 3 GM CSF细胞培养上清可明显刺激小鼠骨髓单个核细胞增殖 ,并能刺激干细胞形成克隆 ,形成克隆数为 (5 4 .6 7± 4 .83)个 ,形成率为 0 .5 4 7%。结论　构建mGM CSF真核表达质粒pcDNA3 GM CSF ,获得稳定表达该基因并具有生物学活性的细胞克隆 ,为制备转GM CSF基因瘤苗 ,探索白血病免疫治疗的可行性奠定基础     

Granulocyte-macrophage colony stimulating factor does not improve neutrophil oxidative metabolism in a patient with variant X-linked chronic granulomatous disease

Variant X-linked chronic granulomatous disease (CGD) is characterised by a decreased but still measurable respiratory burst and cytochrome b content of phagocytes resulting in a clinically milder form of the disease. We examined the in vivo effect of recombinant human granulocyte-macrophage colony stimulating factor (rh-GM-CSF) on the neutrophil functions of a patient treated for liver abscess. The number of white blood cells was markedly increased at the highest dose of GM-CSF injected (30 g/kg per day). This was mainly due to a large increase in eosinophils and to a lesser extent in neutrophils. No change in the deficient neutrophil respiratory burst nitroblue tetrazolium (NBT)-reduction, superoxide (O ₂ ^– )-production and cytochrome b content was observed during 6 weeks of therapy with increasing doses of GM-CSF. No significant clinical improvement of the liver abscess was observed during treatment with GM-CSF.     

烟雾病患儿粒细胞集落刺激因子的变化

目的：探讨粒细胞集落刺激因子（G-CSF）在烟雾病发病机制中的作用。方法：采用酶联免疫吸附法(ELISA)检测20例有症状的烟雾病患儿及20例健康对照儿童的血清G-CSF浓度。结果：健康对照组的血清G-CSF 浓度平均值为23.5±3.8 pg/mL, 烟雾病组平均值为35.7±10.3 pg/mL。烟雾病组的血清G-CSF平均浓度明显高于健康对照组,P<0.01。结论：烟雾病组的血清G-CSF浓度比健康对照组明显升高, 提示G-CSF在烟雾病的发病机制中可能具有重要作用。［中国当代儿科杂志,2010,12（2）：117-119］     

Randomized comparison of antibiotics with and without granulocyte colony-stimulating factor in children with chemotherapy-induced febrile neutropenia: a report from the Children's Oncology Group

PURPOSE: To determine if granulocyte colony-stimulating factor (G-CSF) with empirical antibiotics accelerates febrile neutropenia resolution compared with antibiotics without it. PATIENTS AND METHODS: Eligible children were treated without prophylactic G-CSF and presented with fever (temperature >38.3 degrees C) and neutropenia afterward. Patients with acute myelogenous leukemia and myelodysplastic syndrome were excluded. Assignments were randomized between G-CSF (5 microg/kg/day) or none beginning within 24 hr of antibiotics. Subcutaneous administration was recommended, but intravenous G-CSF was allowed. Patients remained on study until absolute neutrophil count (ANC) >500/microl and > or =48 hr without fever. RESULTS: One of 67 patients enrolled was ineligible, 59 had acute lymphoblastic leukemia (ALL). Thirty-four were assigned to antibiotics, 32 to G-CSF plus antibiotics. Adding G-CSF significantly reduced neutropenia and febrile neutropenia recovery times. Median days to febrile neutropenia resolution was nine earlier with G-CSF (4 vs. 13 days) (P < 0.0001). However, there was no difference in the resolution of fever between arms. Hospitalization median was shorter by 1 day with G-CSF (4 vs. 5 days) (P = 0.04). There was no difference in the duration of IV and oral antibiotic treatment, addition of antifungal therapy, and shock incidence. A trend for decreased incidence of late fever with G-CSF was noted (6.3 vs. 23.5%) (P = 0.08). CONCLUSIONS: Adding G-CSF to empiric antibiotic coverage accelerates chemotherapy-induced febrile neutropenia resolution by 9 days in pediatric patients, mainly with ALL, which results in a small but significant difference in the median length of hospitalization.