微生态学面临"非典"感染的新挑战

微生态学是研究人、动物及植物正常微生物群的新学科。正常微生物群对其宿主不但无害 ,而且有益 ,并具有众多的生理效应。这是正常微生物群与其宿主的长期共生的进化结果 ,是微生态平衡状态的表现。但是 ,在环境发生重大变化时这种微生态平衡就要遭到破坏 ,发生微生态失调 ,并引起宿主各种类型的疾病。微生态失调引起的疾病来源于内源性与外源性两个方面。内源性主要来源于正常微生物群的比例失调、定位转移和二重感染。外源性主要来自外袭菌的侵入 ,形成新的感染。感染如果在群体中有传播性 ,这就是传染病或传播病 (communicabledis ease)…     

微生态制剂的发展现状及其在慢性肝病中的应用

微生态制剂（microecologics）亦称微生态调整剂或生态制剂,是根据微生态学原理,为调整微生态失调,保持微生态平衡,利用对宿主有益无害的正常微生物群成员或其促进物质制成的生态制剂。并具有调整肠道菌群失调,拮抗致病菌,减少肠源性毒素产生和吸收、改善微生态平衡的作用。对急、慢性腹泻和抗生素引起的肠道失调等有良好的预防和治疗作用。     

吸烟对呼吸道感染患者的微生态影响

呼吸道感染是常见病多发病,而呼吸道感染可导致微生态失调。有报道,宿主的任何病理变化都可作为生态失调的微观环境因素。微观环境对正常微生物群的影响是直接的;而且是主要的。为此,我们对吸烟和被动吸烟者的微生态变化及呼吸道感染患者微生态的变化以及二者之间的关系进行了研究。以进一步探讨吸烟对呼吸道感染患者直接或间接的影响。研究结果表明,吸烟及被动吸烟者患反复呼吸道感染的年发生率明显高于不吸烟者。健康对照组与患者口咽部菌群数相比有显著差异,无论是吸烟还是不吸烟的患者菌群含量均高于健康对照组（Ｐ＜００５）。结果表明,吸烟不仅有害于自身健康,而且危害被动吸烟者,其对呼吸道微生态的影响都是一致的,即可导致微生态失调,从而导致呼吸道疾病     

1500例女性阴道微生态状况分析

目的女性阴道微生态状况调查与分析。方法采用阴道pH、阴道涂片Gram染色镜检(菌群密集度、菌群多样性、优势菌、真菌孢子、滴虫和炎性反应等)、阴道微生物功能测定,评估1 500例体检者阴道微生态状况。结果微生态正常830例(55.7%),微生态失调者670例(44.6%)。在670例微生态失调患者中,需氧菌阴道炎156例(23.3%),细菌性阴道病265例(39.6%),外阴阴道假丝酵母菌病31例(4.63%),滴虫性阴道炎2例(0.29%),混合感染216例(32.2%)。结论阴道微生态评价有助于筛查无症状阴道微生态失调患者,对指导临床评价感染及预防阴道感染具有重要的临床意义。     

分子生态制剂的发展

生态制剂(ecologizal preporation,ecolagics或Drobihtics)是微生态学的概念,是利用正常微生物群成员或其促进物质,用以维持微生态平衡(microeu-biosis)的生物制品,其作用在于调整微生态失调(microdysbiosis)。我们从微生态     

质子泵抑制剂对消化道微生态影响的生物学机制

近年来,消化道微生态的相关研究引起广大研究者注意。研究表明质子泵抑制剂(proton pump inhibitors,PPIs)可通过对消化道微生物产生影响,继而引起消化道微生态发生改变。本文分析了PPIs引起消化道微生物变化的相关疾病及原因,发现PPIs通过抑制中性粒细胞的杀菌活性来破坏炎症反应。此外,PPIs抑制胃酸分泌,导致消化道细菌移位、细菌过度生长、肠道通透性增加、肠道蠕动改变和肠道微生物群被破坏,致使肠道黏膜屏障受损和继发性肠道功能失调,由此引起消化道微生态失衡。     

引起机会性感染的常见病原体分析

机会性致病微生物在机体免疫功能正常时不能导致具有明显临床症状的感染性疾病, 但当机体微生态失调或免疫功能受损时, 可导致明显的临床感染性疾病, 甚至危及患者的生命。现代医疗技术的进步使先天性免疫功能缺陷者、肿瘤患者等免疫功能降低者生存期延长, 滥用抗生素致使正常微生态失调, 以及大量耐药变异菌株出现等诸多因素使得临床机会性感染逐渐增多。机会性感染多发生于免疫功能降低者, 可为耐药菌或多重耐药菌感染, 或为正常菌群致病; 临床表现复杂且不典型, 给治疗带来极大困难。了解常见机会性感染病原体及其特点对及时诊断和治疗机会性感染具有重要的临床意义。     

口臭微生态治疗技术研究进展

口臭是指呼吸时排出挥发性硫化物等臭味气体,主要由口腔微生态失调引起,具体为生理性菌群数目减少,产臭类菌群种类和数目增加。口臭是局部口腔或全身系统不良代谢状况的一种表现,临床可根据口腔异味来诊断疾病,并通过口腔微生态的调整来治疗口臭。本研究从口臭与微生态的关系、口臭主要相关微生物等方面进行分析,综述机械、化学和中医药等方法调整口腔微生态来治疗口臭的进展。     

肠道微生态与白血病的研究进展

微生物群与人体的健康密切相关,约20%的恶性肿瘤与微生态失调有关。研究显示肠道微生物可以调节造血,其与血液系统疾病的关系逐渐得到研究者的关注,肠道微生物参与白血病的发生发展,影响白血病的治疗效果。较早的暴露于微生物群是儿童白血病的保护性因素,化疗会引起肠道微生物紊乱,肠道微生物可以改变化疗药物的疗效和毒性,其多样性和组成能够预测化疗相关的并发症,通过微生态制剂和粪菌移植可以减少化疗相关的并发症。本文从肠道微生态与白血病及其并发症的关系,以及调节肠道微生态对白血病的影响两个方面的最新进展进行综述。     

体外牙周微生态模型构建方法及应用研究进展

牙周炎的病因学研究经历了从非特异性菌斑学说、特异性菌斑学说到生态菌斑学说的转变,但其具体的发病机制仍有待进一步研究.近年来,有学者提出了多微生物协同和生态失调模型,病原体组作为疾病病因学中的新概念也逐渐引起重视,这些都提示牙周感染中牙菌斑生物膜与宿主之间存在复杂的相互作用.因此,构建牙周微生态模型对牙周炎病因及防治的研...     

自噬对胞内感染病原菌的清除及促进增殖作用

自噬作为一种新的程序性细胞死亡,其在病原体感染中的地位日益受到广泛关注。自噬在病原体感染中具有"双刃剑"样作用,一方面,机体可利用自噬清除感染入侵的病原体;另一方面,自噬可被某些病原体利用、修饰或干扰,以促进自身在宿主细胞内的存活与增殖。本文拟就近年来自噬与人类疾病关系密切的胞内病原菌感染中的作用及地位进行综述,同时结合本室研究进行一定深入探讨,为探索通过调控及合理利用自噬途径预防和控制感染性疾病的发生发展提供理论依据。     

Restricted expression of herpes simplex virus lytic genes during establishment of latent infection by thymidine kinase-negative mutant viruses.

Infection of cells by herpes simplex virus (HSV) can lead to either lytic, productive infection or nonlytic, latent infection. The factors influencing this infection pathway decision are largely unknown. Thymidine kinase-negative mutant viruses can establish latent infection in neurons of mouse trigeminal ganglia but do not replicate productively in these cells. We show that during the early stages of establishment of latency by these mutants, expression of viral lytic genes is drastically reduced or undetectable as assayed by in situ hybridization. Thus, establishment of latent infection by HSV can occur despite severely restricted levels of lytic gene expression. This suggests that the block to productive replication during establishment of latent infection by HSV occurs before or early during the expression of alpha genes.     

In vitro effect of transforming growth factor-beta on progression of HIV-1 infection in primary mononuclear phagocytes

In vitro-differentiated monocytes can be infected with the monocytotropic isolate of HIV-1/ADA. The infection is characterized by formation of giant cells and production of virus that can be found in cell supernatants or cell-associated. In this study, we demonstrate that the above described parameters of infection can be enhanced by a factor present in acidified M phi supernatants, suggesting that it might be transforming growth factor beta-1 (TGF-beta 1). When recombinant or purified TGF-beta were examined, similar activities were detected. This effect apparently is not because of changes in the cellular phenotype that could favor infection. The effect of TGF-beta is exerted on cells once infection is established or on cells with active virus production. The activity can be also demonstrated using U-937 cells.     

昆虫杆状病毒细胞凋亡抑制基因

杆状病毒感染过程中,可能会诱导产生一条导致细胞凋亡的路径,细胞凋亡是一种程序性细胞死亡。宿主细胞的凋亡可以导致细胞的提前死亡或感染的终止,因此细胞凋亡可以限制病毒在被感染机体中的扩散或限制感染机体的发病。家蚕的杆状病毒拥有两种对抗细胞凋亡死亡的基因,p35和iap(inhibitorofapoptosis),它们可能通过阻止病毒感染引起的细胞凋亡或存在于大量生物体内的各种诱导信号引起的细胞凋亡。     

Further studies on an intermediate host murine model showing that a primary Echinococcus granulosus infection is protective against subsequent oncospheral challenge

We describe the use of a murine model to evaluate resistance against subsequent challenge following a primary infection with oncospheres of Echinococcus granulosus. Mice (Kunming strain) were infected with hatched oncospheres of Echinococcus granulosus; 21 days later a second challenge was given by a different route of infection. A primary infection by intraperitoneal (i.p.) injection stimulated 100 and 90.5% protection in terms of reduced cyst numbers against a secondary infection given subcutaneously (s.c.) or intravenously (i.v.), respectively. A primary infection given s.c. followed by i.p. or i.v. challenge resulted in 84.0 and 100% protection, respectively. Intravenous infection followed by i.p. or s.c. challenge resulted in 98.5 and 69.4% protection, respectively. With the i.v. route of infection, almost all resultant cysts were present in the lungs. The data show that a primary infection with oncospheres can induce total or a high degree of protection against a subsequent challenge and confirms that natural (concomitant) immunity can be stimulated in the intermediate host as the result of a primary infection. This may explain the decline in hydatid infection in sheep older than 2 years in hyper-endemic areas such as those found in Xingjiang, China. These older sheep may have been earlier infected and have subsequently self-cured, with the primary infection stimulating an immune response that protects the intermediate host animals from further infection.     

Infectious mononucleosis and Epstein-Barr virus

Epstein-Barr virus (EBV) is a gamma-herpesvirus that infects over 90% of the human population worldwide. It is usually transmitted between individuals in saliva, and establishes replicative infection within the oropharynx as well as life-long latent infection of B cells. Primary EBV infection generally occurs during early childhood and is asymptomatic. If delayed until adolescence or later, it can be associated with the clinical syndrome of infectious mononucleosis (also known as glandular fever or 'mono'), an illness characterised by fevers, pharyngitis, lymphadenopathy and malaise. EBV infection is also associated with the development of EBV-associated lymphoid or epithelial cell malignancies in a small proportion of individuals. This review focuses on primary EBV infection in individuals suffering from infectious mononucleosis. It discusses the mechanism by which EBV establishes infection within its human host and the primary immune response that it elicits. It describes the spectrum of clinical disease that can accompany primary infection and summarises studies that are leading to the development of a vaccine designed to prevent infectious mononucleosis.     

Immune responses to the major capsid protein during parvovirus infection of rats

Rat virus (RV) is a common parvovirus of laboratory rodents which can disrupt rat-based research. Prenatal or perinatal infection can be pathogenic or lead to persistent infection, whereas infection of adult rats is typically self-limiting. Effects on the host immune system have been documented during RV infection, but little is known about immune responses necessary for viral clearance. Our studies were conducted to identify humoral and cellular responses to the predominant capsid protein, VP2, during experimental infection of adult rats. We observed VP2-specific proliferation, gamma interferon production, and an immunoglobulin G2a humoral response that is maintained for at least 35 days following RV infection. These results strongly suggest the induction of virus-specific Th1-mediated immunity.     

皮肤真菌感染与银屑病的相关性

随着近年来银屑病的发病率逐步增加,关于银屑病病因的研究更加深入。除了遗传、免疫和环境等相关因素,微生物与银屑病的关系也备受关注。关于真菌感染与银屑病的相关性研究始于19世纪,认为糠秕马拉色菌可能是银屑病的致病因子,与银屑病的发生发展密切相关。随后也有研究指出白念珠菌通过超抗原等作用诱发或加重银屑病。但银屑病患者依据自身IL-17增高的特点可以起到一定抵抗微生物感染的作用,因此真菌感染与银屑病的关系暂无定论。随着近年来关于两者之间关系的研究逐渐增多,真菌感染仍是银屑病患者不可忽视的诱发或加重因素之一。明确真菌感染在银屑病患者体内的作用有助于更好地研究银屑病的发病机制以及改善预后。     

微囊泡与病毒感染

微囊泡(microvesicle)是细胞释放到胞外的膜性囊泡,其能将所含的蛋白质、脂类和核酸分子转运给其他细胞,从而介导细胞间通讯。作为严格细胞内寄生的微生物,病毒能利用微囊泡的生物合成和扩散途径进行病毒粒子的组装、出芽和传递,同时将病毒蛋白或基因组包装入微囊泡中。这些病毒修饰的囊泡能介导病毒在机体内的感染和扩散,或导致免疫细胞损伤以及耐受抗体的中和,从而逃避宿主免疫应答,引起持续性感染。重要的是,微囊泡介导的病毒感染打破了对病毒在体内扩散和感染时必须有病毒粒子存在的传统认知。对微囊泡与病毒感染进行综述,以促进对微囊泡介导病毒感染和抑制宿主免疫应答分子机制的了解。     

Animal models of the immunology and pathogenesis of human babesiosis

Animal models of human babesiosis have provided a basic understanding of the immunological mechanisms that clear, or occasionally exacerbate, Babesia infection and those pathological processes that cause disease complications. Human Babesia infection can cause asymptomatic infection, mild to moderate disease, or severe disease resulting in organ dysfunction and death. More than 100 Babesia species infect a wide array of wild and domestic animals, and many of the immunologic and pathologic responses to Babesia infection are similar in animals and humans. In this review, we summarize the knowledge gained from animal studies, their limitations, and how animal models or alternative approaches can be further leveraged to improve our understanding of human babesiosis.