共查询到20条相似文献，搜索用时 593 毫秒
1.
β-干扰素诱导调控和信号转导 总被引：2，自引：2，他引：0
病毒感染哺乳动物细胞后,细胞合成、分泌IFN-β,建立抗病毒状态。IFN-β基因转录诱导主要依靠上游5bp~105bp的增强子区域。dsRNA介导多种转录因子的翻译后修饰,产生生理活性,结合在增强子特异性阳性调节区域。NF-κB结合在PRD(posi-tiveregulatorydomains)Ⅱ区域,转录活化因子2(ATF-2)结合在PRDⅣ区域,IFNregu-latoryfactor(IRF)家族结合在PRDⅢ和PRDⅠ区域,high-mobility-groupproteinI(Y)[HMGI(Y)]结合PRDⅡ和PRDⅣ区域,并与NF-κB相互作用,共同组成增强子,启动IFN-β基因转录,IFN-β合成并分泌到细胞外,与细胞表面IFN-β受体结合,通过Jak-stat信号转导途径发挥生理功能,启动靶基因开始转录,参与机体的非特异性免疫。 相似文献
2.
PrP106-126诱导的神经毒性机制仍不清楚。作者以小鼠成神经瘤细胞N2a为细胞模型,应用WesternBlot方法首次发现PrP106-126导致核转录因子NF-κB的亚单位p65蛋白转移到细胞核内,激活了NF-κB细胞信号分子。转核抑制剂NF-κB SN50预处理细胞减弱了PrP106-126诱导的NF-κB激活程度;并且DNA Ladder凋亡检测及Annexin V-FITC和PI双染流式细胞凋亡检测发现,NF-κB SN50能够抑制p65蛋白转核,在一定程度上也抑制了PrP106-126对N2a细胞的神经毒性效果。结果表明NF-κB信号分子参与了PrP106-126的神经毒性,且NF-κB信号分子的激活对N2a细胞具有促凋亡作用。PrP106-126激活N2a细胞NF-κB信号分子以及NF-κB促凋亡功能的体外研究对于阐明朊病毒病致病机理具有重要意义。 相似文献
3.
4.
5.
核转录因子(nuclear factor-κB,NF-κB)是一个广泛存在于哺乳动物细胞中的转录因子,参与机体的免疫反应、细胞黏附、细胞分化、细胞增殖与凋亡及应激反应等。在奶牛感染乳房炎时,大部分涉及中性白细胞移行和激活的炎性蛋白质的编码基因在他们的启动子区都包含一个可结合NF-κB的κB位点,因此在一定程度上依赖NF-κB调控这些基因的表达。笔者详细的阐述NF-κB基因在奶牛乳房炎发病过程中的特点、作用和表达机制,为从分子水平认识和治疗奶牛乳房炎提供一定的文献支持。 相似文献
6.
7.
Toll样受体(TLR)是宿主细胞识别各种致病微生物的主要模式识别受体,核转录因子-κB(NF-κB)是TLR下游信号通路中的枢纽,TLR-NF-κB信号通路几乎存在于所有细胞中。当细胞受到刺激时会激发TLR-NF-κB信号通路,进而引起炎症、免疫和许多病理反应。益生菌具有提高免疫力、丰富肠道有益菌和抑制肠道疾病炎性因子产生的作用,一些特定的益生菌可以调控TLR-NF-κB信号通路进而调节炎性因子的表达,改善肠道黏膜炎症。本文主要综述了TLR和NF-κB的主要结构功能、TLR-NF-κB信号通路以及益生菌对TLR-NF-κB信号通路的调控作用,为进一步研究益生菌在宿主机体内的作用提供新的思路。 相似文献
8.
《畜牧兽医学报》2015,(12)
为研究丹翘液的体外抗炎作用及其抗炎机制,利用LPS诱导巨噬细胞建立炎症模型,MTT法检测不同浓度丹翘液对RAW264.7细胞活力影响;NO测试盒检测丹翘液对LPS诱导的NO释放量的影响;ELISA方法检测丹翘液对LPS诱导的TNF-α、IL-6和PGE2分泌的影响;RT-PCR方法检测丹翘液对LPS诱导的TNF-α、IL-6、COX-2和iNOS基因转录的影响;Western blot检测对细胞核内NF-κB p65蛋白表达的影响。结果显示丹翘液小于700μg·mL-1对细胞无毒性作用;丹翘液各剂量组(100、300、600μg·mL-1)能不同程度地抑制LPS诱导的NO、PGE2、TNF-α和IL-6的分泌;能显著抑制iNOS、COX-2、TNF-α和IL-6基因转录和细胞核内NF-κB p65蛋白表达。丹翘液的抗炎作用机制可能与抑制NF-κB通路激活,进而抑制炎症介质和炎性细胞因子的转录和表达有关。 相似文献
9.
为了确定猪TLR3基因A1116T错义突变的生物学效应,研究其与猪疾病抗性/易感性的关系,本研究采用重叠延伸PCR和定点突变技术构建不同等位基因的真核表达载体,采用双荧光素酶检测分析系统及Real-timePCR方法在体外培养的细胞中研究不同等位基因在信号转导中的作用。成功地构建了野生型和突变型TLR3的真核表达载体,双荧光素酶检测分析表明突变型活化转录因子NF-κB、激活ISRE的能力都减弱;Real-time PCR分析表明突变型诱导转录IL-6的能力下降。结果表明该点突变影响猪TLR3的信号转导能力。 相似文献
10.
《中国预防兽医学报》2021,(3)
为探究NF-κB信号通路对鸭肠炎病毒(DEV)增殖的影响,本实验分别以不同终浓度的NF-κB信号通路激活剂LPS(2.0μg/mL、4.0μg/mL、6.0μg/mL)和抑制剂SN50(25.0μg/mL、50.0μg/mL、75.0μg/mL)处理鸭胚成纤维(DEF)细胞后,采用CCK8法分析LPS或SN50对DEF细胞活性影响;利用不同浓度的LPS或SN50预处理DEF细胞4 h后,再于12 h~120 h后收获细胞和上清液(未感染DEV);上述经LPS或SN50预处理细胞4 h后接种DEV(MOI 0.01),12 h~120 h后(每间隔12 h)分别收获细胞及上清液,采用荧光定量PCR方法分别检测上述未感染和感染DEV的DEF细胞中NF-κB1基因和DEV NP基因的转录水平;采用ELISA方法分别检测上述未感染和感染DEV的DEF细胞上清液中NF-κB信号通路关键因子(IL-1β、IL-6和MyD88)的表达水平。结果显示:不同浓度的LPS和SN50处理对DEF细胞均无明显毒性作用。荧光定量PCR结果显示,经不同浓度LPS预处理,均能有效提高DEF细胞中NF-κB1基因的转录水平,其中4.0μg/mL LPS处理的DEF细胞中NF-κB1基因转录水平最高;而在LPS预处理再感染DEV后,4.0μg/mL LPS和6.0μg/mL LPS处理的DEF细胞中NF-κB1基因转录水平整体上调(p0.05),2.0μg/mL LPS处理的DEF细胞中NF-κB1基因的转录水平整体下调(p0.05);不同浓度的SN50预处理后,未感染和感染DEV的DEF细胞中,均以50.0μg/mL SN50处理的细胞中NF-κB1基因的转录水平下调效果最好(p0.05)。LPS预处理DEF细胞后感染DEV,12h~84 h DEV NP基因的转录水平均受到明显抑制(p0.01),84 h后2.0μg/mL和6.0μg/mL LPS均会促进DEV NP基因的转录水平;而经SN50预处理DEF细胞后感染DEV,细胞中DEV NP基因的转录水平均显著下降(p0.01)。ELISA结果显示,经LPS预处理后,不感染或感染DEV,DEF细胞中IL-6表达量整体稍呈下降趋势(p0.05),而IL-1β和MyD88的表达则呈无规律变化;经SN50预处理后不感染或感染DEV,DEF细胞中IL-1β、IL-6和MyD88的表达均无规律变化。以上研究结果表明,不同浓度LPS均可促进正常DEF细胞中NF-κB1基因的转录,而DEV则可以阻断低浓度LPS(2.0μg/mL)的这种促进作用。不感染或感染DEV,SN50均于高浓度(50μg/mL和75μg/mL)时才能有效降低NF-κB1基因的转录水平;不同浓度的LPS或SN50均对NF-κB通路关键因子的表达基本无影响;LPS在DEV感染后期才能促进其增殖,而SN50则可以有效抑制DEV的增殖。本研究为阐明NF-κB信号通路与DEV之间的相互作用关系奠定了实验基础。。 相似文献
11.
脂多糖(Lps)是一类具有高度活性的大分子物质,可依赖LBP/CD14系统作用于细胞,特别是单核细胞、巨噬细胞和中性粒细胞(PMNS)等通过一系列胞内信号传导系统诱导细胞产生多种生物活性分子,如:TNF-α,白介素,前列腺素等,在革兰氏阴性菌感染的发病机制中扮演着十分重要的角色,其可激活损伤血管内皮细胞,引起机体产生局部炎症反应和弥散性血管内凝血(DIC)等病理反应,引起发热,呼吸窘迫综合症,心肺功能严重损害及多器官功能衰竭(MOF),甚至引发致死性休克,因此全面了解内毒素的作用机制,研究有效的内毒素拮抗剂,对预防和治疗内毒素(ET)性疾病有重要意义。 相似文献
12.
视黄酸诱导基因Ⅰ(RIG-Ⅰ)为RLRs受体家族的成员,是比较关键的细胞质内病原体识别受体,可识别细胞内的单链、双链等RNA病毒成分,被激活的RIG-Ⅰ受体及其CARD在TRIM25的作用下连接泛素链使其寡聚化,通过与线粒体抗病毒信号蛋白(MAVS)相互作用,激活MAVS及下游转录因子IRF3和NF-κB,从而诱导Ⅰ型干扰素和炎性因子的表达,最终介导宿主的抗病毒免疫应答。鉴于RIG-Ⅰ持续激活可导致炎性因子对自身细胞的损伤,因此RIG-Ⅰ样受体信号通路受到宿主严格的调控。而某些病毒为逃避宿主细胞的免疫应答,进化出多种机制靶向调节RIG-Ⅰ及MAVS,从而阻断信号通路。论文从RIG-Ⅰ识别病毒机制、激活下游信号传导、宿主细胞对信号传导途径的调控以及病毒逃避机制等方面重点阐述RIG-Ⅰ所介导的天然免疫反应。 相似文献
13.
D. M. HAIG 《Research in veterinary science》2001,70(3):205-219
During the co-evolution of viruses with their vertebrate hosts, the DNA viruses have acquired an impressive array of immunomodulatory genes to combat host immune responses and their hosts have developed a sophisticated immune system to contain virus infections. In order to replicate, the viruses have evolved mechanisms to inhibit key host anti-virus responses that include apoptosis, interferon production, chemokine production, inflammatory cytokine production, and the activity of cytotoxic T-cells, natural killer cells and antibody. In addition, some of the viruses encode cytokine or chemokine homologues that recruit or expand cell numbers for infection or that subvert the host cellular response from a protective response to a benign one. The specificity of the viral immunomodulatory molecules reflects the life cycle and the pathogenesis of the viruses. Herpesviruses achieve latency in host cells by inducing cell survival and protecting infected cells from immune recognition. This involves interference with cell signal transduction pathways. Many of the viral immunomodulatory proteins are homologues of host proteins that appear to have been pirated from the host and reassorted in the virus genomes. Some of these have unique functions and indicate novel or important aspects of both viral pathogenesis and host immunity to viruses. The specific example of orf virus infection of sheep is described. 相似文献
14.
Patrick K Lai Michael P Alpers 《Comparative immunology, microbiology and infectious diseases》1979,2(4):565-585
Cell-mediated immune response are now known to be important components of the host response to the Epstein-Barr (EB) herpesvirus. They are also likely to be essential in the control of EB-virus infection. Failure to mount any immune response to EB virus results in loss of control over the multiplication of cells transformed by the virus and gives rise to polyclonal neoplasia. A number of studies, using different preparations of antigen and a variety of assays, have demonstrated specific cell-mediated immune responses to the virus in normal individuals, most of whom by adulthood harbour the virus, and in patients with infectious mononucleosis (IM), where a consistent pattern of response is beginning to be established. However, in patients with Burkitt's lymphoma or nasopharyngeal carcinoma, specific cell-mediated immune responses to the virus have been less easy to detect and difficult to relate in any consistent way to the course of the disease. In this communication we review some of the recent results obtained on cell-mediated immune responses to EB-virus infection, with particular emphasis on the pathogenesis and control of EB-virus-associated diseases. It is clear that EB-virus, though an ubiquitous, almost universal human virus, has a demonstrated potential to produce malignant neoplasia. The oncogenicity of the virus is normally held in check, at least in part through cell-mediated immune mechanisms, so that the usual mode of infection is inapparent or, in some cases, a self-limiting lymphoproliferative disease (IM). Under particular circumstances, Burkitt's lymphoma or nasopharyngeal carcinoma may result, but the role of EB-virus in the pathogenesis of these diseases and especially the part played by cell-mediated immune responses to the virus have by no means yet been elucidated. 相似文献
15.
Bovine respiratory syncytial virus (BRSV) belongs to the pneumovirus genus within the family Paramyxoviridae and is a major cause of respiratory disease in young calves. BRSV is enveloped and contains a negative sense, single-stranded RNA genome encoding 11 proteins. The virus replicates predominantly in ciliated respiratory epithelial cells but also in type II pneumocytes. It appears to cause little or no cytopathology in ciliated epithelial cell cultures in vitro, suggesting that much of the pathology is due to the host's response to virus infection. RSV infection induces an array of pro-inflammatory chemokines and cytokines that recruit neutrophils, macrophages and lymphocytes to the respiratory tract resulting in respiratory disease. Although the mechanisms responsible for induction of these chemokines and cytokines are unclear, studies on the closely related human (H)RSV suggest that activation of NF-kappaB via TLR4 and TLR3 signalling pathways is involved. An understanding of the mechanisms by which BRSV is able to establish infection and induce an inflammatory response has been facilitated by advances in reverse genetics, which have enabled manipulation of the virus genome. These studies have demonstrated an important role for the non-structural proteins in anti-interferon activity, a role for a virokinin, released during proteolytic cleavage of the fusion protein, in the inflammatory response and a role for the SH and the secreted form of the G protein in establishing pulmonary infection. Knowledge gained from these studies has also provided the opportunity to develop safe, stable, live attenuated virus vaccine candidates. 相似文献
16.
17.
Blacklaws BA Berriatua E Torsteinsdottir S Watt NJ de Andres D Klein D Harkiss GD 《Veterinary microbiology》2004,101(3):199-208
Small ruminant lentiviruses (SRLV) are classical slow retroviruses causing chronic inflammatory disease in a variety of target organs. The routes of transmission have been investigated and a large body of evidence has accumulated over many years. The main routes are through ingestion of infected colostrum and/or milk, or through inhalation of respiratory secretions. However, many studies also provide evidence that intrauterine infection may occur, though the extent and significance of this route is controversial. Embryos treated to IETS standards appear to pose very little risk of infection. SRLV have been detected in semen suggesting a potential source of transmission. However, such transmission has not been demonstrated to date. The application of control measures based on this information allows more efficient strategies to be developed which will reduce the rate of transmission. 相似文献
18.
猪的繁殖力是决定其生产效率的重要因素,而病毒感染导致的猪流产问题严重影响猪的繁殖效率。了解猪流产相关病毒的致病机制有助于提高猪的繁殖效率,然而大量的研究主要集中在病毒与宿主的蛋白质或基因组DNA上,近年来,长链非编码RNA （long noncoding RNA,lncRNA）从新的视角揭示了病毒与宿主的相互作用,为研究二者之间的互作关系提供了新的途径。lncRNA是一组长度>200 nt的转录本,主要通过与DNA、RNA、染色质和蛋白质互作发挥功能,在某些发育阶段、组织和疾病状态中发生特异性表达,参与机体的多种调控。lncRNA是调控病毒与宿主相互作用的关键因子,在病毒感染宿主后lncRNA发生差异性表达,对应的靶基因富集到炎症和免疫相关的信号通路,参与机体的炎症、免疫和抗病毒反应。深入了解lncRNA在猪流产相关病毒与宿主之间的调控作用,对预防和治疗病毒感染导致的猪流产具有重要意义。作者对lncRNA及其与猪流产相关病毒的关系、宿主lncRNA与病毒的互作及调控通路展开了综述,并对其存在的问题及应用前景进行了展望,以期为猪的抗病育种、猪流产药物的开发和设计及流产类相关疾病的靶点治疗等提供理论依据。 相似文献
19.
20.
牛疱疹病毒(BHV-1)属于α疱疹病毒亚科的DNA病毒,可引起牛高热、上呼吸道感染和母牛流产。该病毒能在牛的感觉神经节内建立潜伏感染,因此,对于该病毒感染的预防和治疗较为困难。BHV-1除了引起初始感染外,还可通过免疫抑制引起动物继发感染,导致动物死亡。研究发现,病毒入侵牛机体时,病毒囊膜糖蛋白在病毒与细胞间相互作用的过程中发挥了重要作用。论文对牛疱疹病毒1型主要囊膜糖蛋白(包括gB、gD、gN)的结构特征和生物学特征加以归纳总结,为该病毒的感染特性研究和预防提供参考。 相似文献