Bone marrow colonies: stimulation in vitro by supernatant from incubated human blood cells

A substance which stimulates growth of granulocytic and mononuclear cell colonies from mouse and human bone marrow was produced by incubated human blood cells. It is resistant to heat and freezing and is not dialyzable. Intact irradiated and unirradiated cells had very little activity, and sonically disrupted cells had no activity. The addition of plasma or sonically disrupted cells to the cell supernatant decreased its activity.     

Delayed hypersensitivity: bone marrow as the source of cells in delayed skin reactions

Adult Lewis rats were thymectomized, irradiated, and restored with bone marrow from allogeneic (or F(1)) donors. They were passively sensitized to tuberculin by a subsequent transfer of Lewis lymph node cells and were given intradermal skin tests with tuberculoprotein. In 24-hour skin reactions the majority of cells, in successive experiments, were shown to be allogeneic (or F(1)) with the use of isoantibody against the antigens of the transplanted marrow cells and by the indirect fluorescent antibody technique. Our results demonstrate that the non-specific cells making up a large proportion of the infiltrating elements in tuberculin skin reactions probably originate in the bone marrow.     

Differentiation of murine bone marrow stem cells in vitro: long-term growth promoted by a lymphocyte-derived mediator

In attempts to induce differentiation of lymphoid cells from hematopoietic stem cells in vitro, the effects of allogeneic effect factor on the growth of murine bone marrow cultures were studied. Allogeneic effect factor is a soluble mediator derived from mixed secondary murine leukocyte cultures. For several weeks it supported the growth of bone marrow cultures, as indicated by the maintenance of stem cell activity, cellular proliferation, and heterogeneity. Another lymphokine, T cell growth factor, did not, Pre-T lymphocytes could be detected in these cultures for several weeks.     

Homeostasis of the antibody response: immunoregulation by NK cells

When injected into mice, the synthetic double-stranded polynucleotide poly(inosinic) X poly(cytidylic) acid induces high natural killer (NK) cell activity within 4 to 12 hours. Induction of NK activity in mice immunized 2 or 3 days previously, or the addition of NK cells to cultures immunized in vitro 2 or 3 days previously, promotes early termination of the ongoing primary immunoglobulin M antibody response. A target for NK cells is a population of accessory cells that has interacted with antigen and is necessary for sustaining the antibody response. The inference is strong that NK cells induced normally by immunization also terminate the usual antibody response in vivo by elimination of antigen-exposed accessory cells.     

Cultured cells of white pine show genetic resistance to axenic blister rust hyphae

Hypersensitive resistance to axenically cultured Cronartium ribicola was displayed by subcultured callus of Pinus lambertiana. Cellular resistance to a destructive rust disease can now be studied at the macromolecular level through use of cloned cells of both host and pathogen in a system amenable to emerging recombinant DNA technology.     

MHC class I deficiency: susceptibility to natural killer (NK) cells and impaired NK activity.

The role of major histocompatibility complex (MHC) class I expression in natural killer (NK) cell target recognition is controversial. Normal T cell blasts from MHC class I-deficient mutant mice were found to serve as target cells for NK cells in vitro, which suggests that MHC class I molecules are directly involved in NK cell recognition. Spleen cells from the mutant mice were deficient in their ability to lyse MHC class I-deficient target cells or NK-susceptible tumor targets, and mutant mice could not reject allogeneic bone marrow. Thus, class I molecules may participate in the positive selection or tolerance induction of NK cells.     

Disentangling genetic variation for resistance and tolerance to infectious diseases in animals

Hosts can in principle employ two different strategies to defend themselves against parasites: resistance and tolerance. Animals typically exhibit considerable genetic variation for resistance (the ability to limit parasite burden). However, little is known about whether animals can evolve tolerance (the ability to limit the damage caused by a given parasite burden). Using rodent malaria in laboratory mice as a model system and the statistical framework developed by plant-pathogen biologists, we demonstrated genetic variation for tolerance, as measured by the extent to which anemia and weight loss increased with increasing parasite burden. Moreover, resistance and tolerance were negatively genetically correlated. These results mean that animals, like plants, can evolve two conceptually different types of defense, a finding that has important implications for the understanding of the epidemiology and evolution of infectious diseases.     

gamma-Glutamyl transpeptidase in isolated brain endothelial cells: induction by glial cells in vitro

The endothelia of microvessels isolated from mouse brain by mechanical means are rich in gamma-glutamyl transpeptidase; however, the enzyme often disappears when the cells migrate or proliferate from the microvessel isolates. In an endothelial cell line derived from similar isolates and negative for gamma-glutamyl transpeptidase, the enzyme could be induced in the endothelial cells when they were cocultured with glial cells. Thus there may be a requirement for continuous induction of gamma-glutamyl transpeptidase in brain microvessels by adjacent glial cells.     

Glucose-6-phosphate dehydrogenase deficient red cells: resistance to infection by malarial parasites

Erythrocyte mosaicism occurs in females heterozygous for glucose-6-phosphate dehydrogenase deficiency. In blood from female children with acute Plasmodium falciparum malaria the parasite rate was 2 to 80 times higher in normal than in deficient erythrocytes. This may be the mechanism whereby the gene for glucose-6-phosphate dehydrogenase deficiency confers selective advantage against malaria to heterozygous females, and thus may have attained the polymorphic frequency occurring in populations living in areas with endemic malaria.     

应用离体叶片法鉴定菠萝资源心腐病抗性

心腐病是对菠萝造成严重危害的病害之一,是由烟草疫霉Phytophthora nicotianae引起的土传病害,较 难防治.为筛选出可在生产或育种中利用的抗病材料,采用离体叶片法鉴定了117 份菠萝材料对心腐病的抗性.结 果显示:不同菠萝材料之间的抗性差异较大袁鉴定出高抗材料38 份尧抗病材料24 份尧中抗材料17 份尧感病材料38 份,分别占供试材料的32.48%尧20.51%尧14.53%和32.48%袁这表明现有菠萝材料中有丰富的抗心腐病资源,可供菠萝 育种应用.     

BMP4在诱导骨髓间充质干细胞向生殖细胞分化中的作用

为了探讨骨形态发生蛋白4(bone morphogenetic protein 4,BMP4)在诱导骨髓间充质干细胞(bone marrow mesenchymal stem cells,BMSCs)向生殖细胞分化中的作用,将全骨髓培养法获取小鼠BMSCs,在含10%胎牛血清(fetal bovine serum,FBS)的DMEM培养液中培养传代;取生长状态良好的第三代(P3)BMSCs,分别添加不同浓度(5、10、20、40和80ng·mL~(-1))的BMP4作为实验组,未添加BMP4为对照组。4d后,MTT法和台盼蓝染色检测细胞的增殖率和存活率,实时定量PCR(RT-qPCR)检测生殖细胞阶段特异性基因(Oct4、Dazl、Fragilis、Mvh、Nobox、Stella、Stra8和Gdf9)的表达。结果发现,BMP4浓度为5~20 ng·mL~(-1)时细胞存活率和增殖率最高;BMP4浓度为20 ng·mL~(-1)组Mvh、Fragilis、Oct-4、Dazl及Stella表达水平最高,均显著高于对照组(P0.05);Nobox表达水平则在BMP4浓度40ng·mL~(-1)组最高,且各浓度组均显著高于对照组(P0.05);各浓度BMP4组Stra8和Gdf9的表达水平均与对照组间无显著性差异(P0.05)。此结果提示,BMP4浓度在20 ng·mL~(-1)时,BMSCs的存活率、增殖率及原始生殖细胞特异性基因的表达最高;BMP4在诱导间充质干细胞向生殖细胞分化过程中起重要作用。     

Homograft target cells: contact destruction in vitro by immune macrophages

Specific adherence of immune macrophages to monolayers of target cells is a passive phenomenon which represents only the first step in the mutually destructive interaction of immune macrophages and target cells. A specific hemagglutinin, responsible for specific adherence, was eluted from well-washed immune macrophages by heat treatment. The nature of the events in the interaction subsequent to adherence are unknown, but apparently demand the biosynthetic activities of the immune macrophage.     

猪圆环病毒2型体外诱导RAW264.7细胞氧化应激模型的建立

[目的]探讨猪圆环病毒2型(PCV2)感染量、感染时间与被感染RAW264.7细胞活性氧水平动态变化的相关性,为建立RAW264.7细胞氧化胁迫体外模型提供参考依据.[方法]PCV2原液调至5×106/mL,经10、102、103和104倍稀释(10-1、10-2、10-3和10-4释度)后,感染作用RAW264.7细胞2h,弃病毒液,加入含5% FBS的DMEM培养液继续培养,分别于第4、8、12、24和48 h收集细胞上清液或细胞,测定一氧化氮(NO)、活性氧自由基(ROS)、还原型谷胱甘肽(GSH)、氧化型谷胱甘肽(GSSG)、黄嘌呤氧化酶(XOD)、髓过氧化物酶(MPO)和诱生型一氧化氮合酶(iNOS)等指标.[结果]10-1PCV2感染RAW264.7细胞后能有效升高细胞NO、ROS水平,降低细胞GSH水平和GSH/GSSG,升高细胞XOD、MPO和iNOS活性,表明以10-1pcv2感染RAW264.7细胞一定程度上能改变细胞氧化还原状态,诱导细胞产生氧化应激.[结论]PCV2感染能诱导RAW264.7细胞发生氧化应激,并确立10-1 PCV2(5× 105/mL)体外感染RAW264.7细胞4~24 h是建立RAW264.7细胞氧化胁迫模型的最佳条件.     

猪骨髓基质细胞的分离培养及生物学特性研究

【目的】探讨猪骨髓基质细胞(bone marrow stromal cells,BMSCs)的体外分离培养方法,并对猪BM-SCs的生物学特性进行研究,旨在建立一种稳定的体外培养猪BMSCs的方法体系。【方法】分离刚出生猪的BMSCs进行体外培养,传代,分别观察原代及传代细胞的形态和分化特征,绘制生长曲线,测定细胞分裂指数和贴壁率。采用细胞免疫化学染色对碱性磷酸酶(ALP)进行检测,以确定成骨分化能力,并通过免疫组化法对表面分子CD44、CD34进行染色鉴定。【结果】猪BMSCs体外生长良好,细胞接种后1~2 d生长缓慢,2~5 d进入对数生长期,6 d后细胞数开始下降;猪BMSCs在第4天分裂指数最高,约为10%;猪BMSCs传代后10 h贴壁率最高,达90%以上。猪BMSCs ALP染色阳性率达到75%;CD44阳性率可达98.83%,而CD34在第2代后消失;猪BMSCs在第5代以前生长形态稳定,培养至7代后,衰老现象严重。【结论】该方法分离的猪BMSCs早期生长性状稳定,增殖速度快,并获得了高纯度的猪BMSCs,据此建立了一种稳定的体外培养猪BMSCs的方法体系。     

甜瓜白粉病抗性遗传机制研究

两组甜瓜白粉病抗感杂交组合的遗传模型均符合B-1模型,即甜瓜白粉病抗性是由两对主基因控制,且两主基因表现为加性-显性-上位性效应。组合(7-2)×(7-1)主基因遗传率,2004年秋为96.32%,2005年春为93.27%;组合(7-2)×(7-3)的主基因遗传率,2004年秋为98.22%,2005年春为94.67%。主基因遗传率较高。     

Host resistance to lung infection mediated by major vault protein in epithelial cells

The airway epithelium plays an essential role in innate immunity to lung pathogens. Ribonucleoprotein particles primarily composed of major vault protein (MVP) are highly expressed in cells that encounter xenobiotics. However, a clear biologic function for MVP is not established. We report here that MVP is rapidly recruited to lipid rafts when human lung epithelial cells are infected with Pseudomonas aeruginosa, and maximal recruitment is dependent on bacterial binding to the cystic fibrosis transmembrane conductance regulator. MVP was also essential for optimal epithelial cell internalization and clearance of P. aeruginosa. These results suggest that MVP makes a substantial contribution to epithelial cell-mediated resistance to infection.