马红球菌感染的研究进展

马红球菌是一种机会致病菌。近来随着免疫缺陷人群的增多和认识的深入,对该菌感染的报道日益增多。本文就人类马红球菌感染的微生物学、感染途径、致病机制、病理学变化、临床表现、治疗和预防作一综述。     

铜绿假单胞菌与机体免疫的相互关系

铜绿假单胞菌是导致许多急性和慢性感染的重要细菌,在机械通气或某些免疫缺陷的患者中常常导致严重的感染。在其所造成的感染中,随着感染的持续发展,铜绿假单胞菌极易形成生物膜。生物膜是一个具有结构性、协调性和功能性的高度组织群体,生物膜细菌的生物学特性与浮游菌显著不同,其环境适应能力更强,不仅可以防止抗生素的杀灭,还能逃避宿主免疫,使得铜绿假单胞菌相关感染的临床治疗变得更加棘手。本文主要综述铜绿假单胞菌如何逃避宿主免疫和机体在铜绿似单胞菌感染时的免疫反应及在免疫方面的治疗进展。     

温度变化触发脑膜炎奈瑟菌的免疫逃逸

<正>脑膜炎奈瑟菌有好几种策略来逃逸补体介导的杀死作用,而这些使其有能力引起败血症和脑膜炎。这种脑膜炎球菌主要是人咽喉部的专性共栖菌,但它为什么进化了精巧的机制来逃逸宿主的免疫力尚不清楚。此文作者阐述了脑膜炎球菌免疫逃逸和对环境温度升高引起的补体增多发生抵抗的机制。作者在荚膜生物合成、H因子结合蛋白表达和脂多糖唾液酸化所需基因的5'非翻译区,鉴定了3个独立的RNA热传感物,它们是脑膜炎球菌抗免疫杀死必需的成分。因而升高的温度(发生在炎症期间)成     

天然免疫系统与新生隐球菌感染

天然免疫系统是宿主免疫防御体系中对抗微生物侵染的第一道屏障。天然免疫细胞通过模式识别受体(pattern recognition receptors,PRRs)识别外源微生物及其成分,其中NOD样受体(NOD like receptors,NLRs)是定位于细胞内的一类PRRs。NLRP1、NLRP3和NLRC4等NLRs家族成员可以形成叫做炎症小体的分子复合体,介导炎症因子IL-1β和IL-18的成熟。目前已经确定多种炎症小体参与抗真菌的免疫反应。新生隐球菌是一种重要的条件性致病真菌,该菌主要感染AIDS等免疫缺陷患者,感染死亡率很高。目前,人们对天然免疫系统抗新生隐球菌的机制有了一定的了解。该文将对宿主抗新生隐球菌的天然免疫机制进行总结。     

铜、铁离子代谢调节隐球菌致病力及宿主免疫的研究进展

金属离子参与真菌和哺乳动物众多重要的生长代谢过程。隐球菌利用金属离子参与毒力因子的形成;宿主利用金属离子进行自身代谢,增强机体免疫,抵御隐球菌感染。因此深入研究隐球菌金属离子代谢,以及探索宿主利用金属离子抵御隐球菌感染的调控机制是至关重要的,可为真菌感染的治疗提供理论依据。     

幽门螺杆菌感染时宿主免疫应答的特征

幽门螺杆菌感染可通过各种致黏膜炎症信号诱导宿主产生较强的免疫反应,但宿主免疫应答非但不能有效地清除感染,反而促进炎症反应而导致病情的加剧。本文综述了幽门螺杆菌感染所致宿主免疫应答以及该菌长期定居胃黏膜和致炎症的机制。     

隐球菌形态学变化及其致病机制

致病真菌在与宿主相互作用过程中可能发生形态学变化,如菌丝形成.这种形态学变化有利于病原菌适应不同的外界环境,使其在宿主体内生存.外有荚膜包裹的隐球菌是隐球菌病的致病真菌.该菌可通过孢子吸人方式侵入宿主体内,其后又能通过增加自身荚膜厚度和形成巨大菌体来抵抗和逃避宿主的免疫防御功能.对隐球菌形态学变化意义的理解,有助于了解该病的致病机制,从而推动临床诊治发展.     

细菌CRISPR-Cas 系统功能及其与噬菌体相互作用

摘要:近来研究发现,细菌CRISPR-Cas 系统在宿主菌抵抗可移动基因元件(mobile genetic elements,MGEs)的过程中发挥重要作用。CRISPR-Cas还参与宿主菌群体行为和毒力基因调控、DNA修复和基因组进化过程。本文着重综述细菌CRISPR-Cas系统的结构、类型、作用机制及其适应性免疫之外的其他功能(如对内源性基因表达的调控、促进基因组进化、DNA修复等);概述噬菌体抵抗CRISPR-Cas系统的机制,并对噬菌体-宿主菌相互作用进行探讨和展望。     

贝氏柯克斯体感染对宿主细胞免疫调控的研究进展

Q热的病原体贝氏柯克斯体是专性细胞内寄生菌,该菌的高致病性和对环境、理化因素的高抵抗力使其成为重要的生物战剂/生物恐怖剂.进入宿主细胞后,Cb能在巨噬细胞内生长繁殖,导致单核细胞朝向非典型M2分化;它通过抑制树突细胞的成熟,干扰细胞因子的正常分泌等多种方式调控宿主细胞的免疫机制,从而逃避机体对其的免疫攻击.     

细菌的噬菌体感染抗性机制

噬菌体广泛存在于生态环境中。细菌在与噬菌体长期的共进化过程中,衍化出了多种针对噬茵体感染的抗性机制。我们从宿主菌的抑制吸附、阻止噬菌体DNA注入、切断噬菌体DNA和影响其功能及流产感染等方面,对宿主菌抵抗噬菌体感染的机制进行了综述。     

布鲁氏菌逃逸宿主的抗感染免疫机制

布鲁氏菌病是由布鲁氏菌引发的世界范围的人兽共患传染病。布鲁氏菌为兼性胞内寄生菌,无典型的毒力因子,但却有很强的致病性,常引发人和动物的慢性感染。逃逸宿主的抗感染免疫反应是慢性感染的先决条件,这种能力对于布鲁氏菌的毒力来说似乎也越来越关键。作为成功的致病性病原菌,布鲁氏菌采用"隐秘的"策略以逃避或抑制固有免疫、调节适应性免疫,从而在宿主细胞内建立长期的持续性感染。本文将围绕布鲁氏菌逃逸宿主的抗感染免疫的分子机制进行阐述,旨为阐明布鲁氏菌毒力的新见解,这很可能为布病的预防开辟新的途径。     

Concomitant and protective immunity in mice exposed to repeated infections with Echinostoma malayanum

Concomitant immunity and its consequence against infection play roles in regulating worm burdens in helminthiasis. Under natural conditions, this immunity is generated by exposure to repeated low dose or trickle infection. In this study, concomitant immunity was induced in mice exposed repeatedly to infection with Echinostoma malayanum and its protective effect on a challenge infection evaluated. A profile of worm burden from exposure to 10 metacercariae/mouse/week rose rapidly during the first 2 weeks reaching a plateau from week 3 to 8 post infection. Based on a cumulative dose of infection, worm recoveries were around 75% in the first 2 weeks, dropped to 50% at week 3 and 19% at week 8. After week 2, adult worm burden was constant and no juvenile worms were found after week 3 of the experiment. To examine the effect of resistance against reinfection, mice in the experimental group were primarily infected with 10 metacercariae/week for 5 weeks, treated with praziquantel and were challenged with 75 metacercariae/animal. The number of worms recovered from the experimental groups was significantly lower than that from naïve control groups beginning from 24 h to 28 days post challenge. The worms in the experimental group showed growth retardation and the proportion of adult worms was lower than that in the control animals especially during the first 3 weeks of the experiment. Parasite fecundity was also suppressed compared with that in the control group. The selective effects of protective immunity on establishment, growth, and fecundity of challenged worms affected the population dynamics of E. malayanum which is a similar phenomenon to concomitant immunity in schistosomiasis.     

Primary structure of apolipophorin-III from the greater wax moth,Galleria mellonella

The complete amino acid sequence of apolipophorin-III (apoLp-III), a lipid-binding hemolymph protein from the greater wax moth,Galleria mellonella, was determined by protein sequencing. The mature protein consists of 163 amino acid residues forming a protein of 18,075.5 Da. Its sequence is similar to apoLp-III from other Lepidopteran species, but remarkably different from the apoLp-IIIs of insects from other orders. As shown by mass spectrometric analysis, the protein carries no modifications. Thus, all of its known physiological functions, including its recently discovered immune response-stimulating activity, must reside in the protein itself.     

Primary structure of apolipophorin-III from the greater wax moth,Galleria mellonella

The complete amino acid sequence of apolipophorin-III (apoLp-III), a lipid-binding hemolymph protein from the greater wax moth,Galleria mellonella, was determined by protein sequencing. The mature protein consists of 163 amino acid residues forming a protein of 18,075.5 Da. Its sequence is similar to apoLp-III from other Lepidopteran species, but remarkably different from the apoLp-IIIs of insects from other orders. As shown by mass spectrometric analysis, the protein carries no modifications. Thus, all of its known physiological functions, including its recently discovered immune response-stimulating activity, must reside in the protein itself.     

Detection of cellular immunity with the soluble antigen of the fungus Sporothrix schenckii in the systemic form of the disease

Sporothrix schenckii is the etiologic agent of sporotrichosis, a mycosis of world-wide distribution more commonly occurring in tropical regions. The immunological mechanisms involved in the prevention and control of sporotrichosis are not fully understood but apparently include both the humoral and cellular responses. In the present investigation, cellular immunity was evaluated by in vivo and in vitro tests in mice infected with yeast-like forms of S. schenckii. The disease developed systemically and cellular immunity was evaluated for a period of 10 weeks. The soluble antigen utilized in the tests was prepared from yeast form of the fungus through the sonication (20 min: 10 sonications at 50 W at 2-min intervals). Delayed hypersensitivity and lymphocyte transformation tests showed that the cellular immune response was depressed between the 4th and 6th week of infection when the animals were challenged with the soluble fungal antigen. This depression frequently indicates worsening of the disease, with greater involvement of the host. This is a promising field of research for a better understanding of the pathogeny of this mycosis.     

Cell-mediated immune responses (CMIR) to Rhinosporidium seeberi in mice

There is no published data on Cell Mediated Immune Responses in experimental animals to Rhinosporidium seeberi the causative agent of human and animal rhinosporidiosis. The quantitative mouse foot-pad model was used to assay the Delayed-Type Hypersensitivity (DTH) cell-mediated immune response to extracts of purified endospores and sporangia of R. seeberi. Histological examination was used to confirm that the foot-pad reactions were compatible with DTH reactions in the mouse. We report that sonically disintegrated rhinosporidial endospores/sporangia induced DTH responses in the foot-pads of sensitized mice which were comparable in intensity and histological profile to that induced by sheep red blood cells in SRBC sensitized mice. Anti-rhinosporidial antibody was also induced. Filtrates of the soluble antigens in sonicated suspensions failed to evoke a DTH-foot-pad (DTH-FP) response in sensitized mice although an anti-rhinosporidial antibody response to this preparation was detected. Prolonged pre-treatment with sonicated suspensions of endospores and sporangia resulted in a decrease of DTH reactivity as compared with reactions following pre-treatment of a shorter duration. This revised version was published online in June 2006 with corrections to the Cover Date.     

Silencing the genes for dopa decarboxylase or dopachrome conversion enzyme reduces melanization of foreign targets in Anopheles gambiae

The production of melanin is a complex biochemical process in which several enzymes may play a role. Although phenoloxidase and serine proteases are clearly key components, the activity of other enzymes, including dopa decarboxylase and dopachrome conversion enzyme may also be required. We tested the effect of knockdown of gene expression for these two enzymes on melanization of abiotic targets in the mosquito, Anopheles gambiae. Knockdown of dopa decarboxylase and dopachrome conversion enzyme resulted in a significant reduction of melanization of Sephadex beads at 24 h after injection. Knockdown of a third enzyme, phenylalanine hydroxylase, which is involved in endogenous production of tyrosine, had no effect on bead melanization. Quantitative analysis of gene expression demonstrated significant upregulation of phenylalanine hydroxylase, but not the other two genes, following injection.     

Sequence, expression and localization of the immunity protein for colicin B

Summary Cells of Escherichia coli containing the cbi locus on plasmids are immune to colicin B which kills cells by dissipating the membrane potential through pore formation in the cytoplasmic membrane. The nucleotide sequence of the cbi region was determined. It contains an open reading frame for a polypeptide consisting of 175 amino acids. The amino acid sequence is homologous to the primary structure of the colicin A immunity protein. This, and the strong homology between the pore-forming domains of colicins A and B suggests a common evolutionary origin for both colicins. The immunity protein could be identified following strong overexpression of cbi. The electrophoretically determined molecular weight of 20 000 was close to the calculated molecular weight of 20 185. The protein contains four large hydrophobic regions. The immunity protein was localized in the membrane fraction and was mainly contained in the cytoplasmic membrane. It is proposed that the immunity protein inactivates the colicin in the cytoplasmic membrane.     

一株猪肠道Lactobacillus animalis LGM对结肠炎小鼠Th细胞分化转录因子基因表达的影响

【目的】从体外和体内研究Lactobacillus animalis LGM对Th细胞分化转录因子T-bet、GATA-3、ROR-γt和Foxp3的调节作用,以及探究L. animalis LGM对小鼠结肠炎的影响。【方法】本试验采用改良型的Hungate滚管技术从猪结肠内容物中分离一株L. animalis LGM,根据其16S rRNA序列进行鉴定。收集L. animalis LGM培养液上清,与细菌脂多糖(LPS,2μg/mL)同时孵育Caco-2细胞24 h,体外研究L. animalis LGM对Caco-2细胞内Th细胞分化转录因子(T-bet,GATA3,ROR-γt和Foxp3) mRNA表达的影响;配制L. animalis LGM细菌悬液,研究L. animalis LGM灌胃对DSS诱导结肠炎小鼠症状及结肠Th细胞分化转录因子和细胞因子(IFN-γ,IL-4,IL-17和IL-10) mRNA表达的影响,表达结果采用荧光定量PCR法检测。【结果】与对照组相比,L.animalisLGM培养液上清显著上调Caco-2细胞内ROR-γt与Foxp3 mRNA表达(P0.05),显著下调GATA3、IL-4、IL-17和TGF-βmRNA表达(P0.05)。L. animalis LGM灌胃显著上调小鼠结肠内ROR-γt和Foxp3的表达(P0.05),显著降低了促炎因子IL-4和IL-17的表达(P0.05),阻止了小鼠结肠长度缩短(P0.05)。【结论】猪肠道分离L. animalis LGM表现出对Th细胞分化转录因子的选择性调节,显著上调Caco-2细胞及结肠炎小鼠ROR-γt与Foxp3mRNA表达。降低DSS诱导结肠炎小鼠炎症水平,对DSS诱导结肠炎起保护作用,有助于维护肠道环境稳态。