脆弱拟杆菌(BF839)菌液的临床应用研究

作者从儿童粪便中分离出一株无毒无遗传毒性的菌株，定名为BF839。临床观察表明该菌菌液有调整菌群、抑制肠道致病菌生长、增强免疫、促进儿童生长发育、防治肠道和呼吸道疾病、增加食欲、充沛精力、改善睡眠等作用。     

高效微生物饲料添加剂

一、国内外研究应用现状 微生物添加剂(Microbial additives)是对包括益生素(probiotics)、微生态制剂在内的有益微生物制剂的一种广义和通俗的解释,又名活菌剂、生菌剂、促生素、利生素等。它的核心含义是指摄入动物体内参与肠道内微生物平衡的具有直接通过增强动物对胃肠内有害微生物群落的抑制作用,或通过增强非特异或特异性免疫功能来预防疾病,     

益生菌抗轮状病毒感染免疫调节机制的研究进展

轮状病毒(rotavirus,RV)是引起婴幼儿和幼龄动物腹泻的主要病原体之一,全世界每年因感染RV而死亡的婴幼儿约为21. 5万人,目前尚无抗RV特效药。研究表明,益生菌作为对宿主有益的一类微生物,可缓解由RV引起的腹泻,并可通过下调A20表达、降低TLR3诱导的小肠损伤和上调细胞因子表达等,提高机体抗RV免疫状态。本文对益生菌在抗RV感染及其对宿主免疫调节作用等方面作一综述,为RV的防治提供参考。     

应用脾直接免疫法制备HCG单克隆抗体

应用脾直接免疫方法制备HCC单克隆抗体,获得了高效价BALB/c小鼠抗血清。稀释到1:150倍仍为强阳性(ELISA法)。采用上述方法用HCG免疫小鼠的脾细胞与NS-1细胞融合生成的杂交瘤细胞所分泌的抗体效价为1:6000以上(ELISA法)。脾直接免疫方法与传统免疫方法相比较,操作简便,免疫时间短,节省抗原。利用此方法获得分泌特异性抗体的杂交瘤与同一抗原,按传统方法免疫动物获得的杂交瘤所分泌的抗体,在效价上和抗体特异性上没有差别。是一种很实用的免疫方法。     

基于RIG-I的狂犬病病毒免疫逃逸机制

狂犬病是重要的人兽共患疾病,在我国,每年约有2000～3000人死于狂犬病。固有免疫是机体针对病毒等病原的第一道非特异的防线,同时,也对特异性的获得性免疫应答产生影响。目前,固有免疫中RIG-I通路及其抗病毒作用机制研究深入广泛。狂犬病病毒进化中获得诸多针对宿主特别是固有免疫应答的逃逸机制,针对该机制的研究对于狂犬病的预防、诊断及治疗具有重要意义,同时,也为其他病毒的免疫逃逸相关研究奠定基础。     

免疫分析在农药研究中的应用

免疫分析是利用免疫反应的特异性和示踪物的灵敏性进行物质超微量分析的传统方法。简述了免疫分析在农药中毒诊断、农药作用机理研究、农药残留分析、农药抗性测定及农药代谢研究中等方面的应用。     

赢创与柏斯托签署联合研发协议，开发动物营养新产品

<正>日前,赢创和柏斯托公司签署了一项联合研发协议,旨在共同开发动物营养新产品,并进一步探讨未来深度商业合作方案。该项合作将赢创独特的肠道健康模拟系统和益生菌产品组合,与柏斯托高效安全的酸化剂酯化创新技术相结合,通过双方先进的科学技术和实践经验,实现突破性的创新,以满足未来畜牧业的发展需求。具体来说,双方将联合开发改善动物肠道健康的产品,并确保     

应用鸡卵细胞大量制备多克隆抗体

用三种不同来源的抗原(基因工程HBVe、HCV核心区抗原和GM—CSF)免疫鸡,观察血清及卵黄中特异性抗体的应答,结果经免疫的鸡对这3种抗原均有免疫应答,所产卵的卵黄中可测出大量的有活性的抗体。提示鸡源性抗体在生物制品开发应用方面有一定的前景。     

抗人膀胱癌抗独特型抗体诱导特异性迟发过敏反应的研究

目的研究对抗人膀胱癌抗独特型抗体(BC2)诱导的特异性迟发过敏反应(DTH)。方法经过BC2免疫的小鼠,用膀胱癌细胞系进行脚掌注射攻击后,测定脚掌水肿厚度判定DTH反应强度,并进行病理学检查。结果BC2诱导的DTH平均水肿厚度为0·95mm,与膀胱癌组织抗原组比较差异无显著意义(P>0·05);免疫鼠对胃癌细胞攻击呈阴性反应;BC2诱导的病变内可见大量炎性细胞,呈弥漫性浸润。结论BC2具有抗原模拟作用,可诱导特异性的DTH反应,可能成为膀胱癌防治的新途径。     

高效价特异性HER2ME抗体的制备及鉴定

目的　制备高特异性HER2ME(Multi epitopeofhumanepidermisgrowthfactorreceptor 2 )抗体。方法将表达HER2ME基因的pcDNA3质粒与CpG混合免疫C5 7小鼠。结果　得到了HER2ME蛋白特异性抗血清。该血清与普通蛋白抗原免疫产生的血清相比 ,抗体特异性极高。未经纯化进行免疫印迹实验 ,显示出高度特异性。结论　表达质粒与CpG混合免疫可简单快速获得高特异性HER2ME抗体。     

Native and Engineered Probiotics: Promising Agents against Related Systemic and Intestinal Diseases

Intestinal homeostasis is a dynamic balance involving the interaction between the host intestinal mucosa, immune barrier, intestinal microecology, nutrients, and metabolites. Once homeostasis is out of balance, it will increase the risk of intestinal diseases and is also closely associated with some systemic diseases. Probiotics (Escherichia coli Nissle 1917, Akkermansia muciniphila, Clostridium butyricum, lactic acid bacteria and Bifidobacterium spp.), maintaining the gut homeostasis through direct interaction with the intestine, can also exist as a specific agent to prevent, alleviate, or cure intestinal-related diseases. With genetic engineering technology advancing, probiotics can also show targeted therapeutic properties. The aims of this review are to summarize the roles of potential native and engineered probiotics in oncology, inflammatory bowel disease, and obesity, discussing the therapeutic applications of these probiotics.     

Effect of Microbiome on Non-Alcoholic Fatty Liver Disease and the Role of Probiotics,Prebiotics, and Biogenics

Non-alcoholic fatty liver disease (NAFLD) is a leading cause of liver cirrhosis and hepatocellular carcinoma. NAFLD is associated with metabolic disorders such as obesity, insulin resistance, dyslipidemia, steatohepatitis, and liver fibrosis. Liver-resident (Kupffer cells) and recruited macrophages contribute to low-grade chronic inflammation in various tissues by modulating macrophage polarization, which is implicated in the pathogenesis of metabolic diseases. Abnormalities in the intestinal environment, such as the gut microbiota, metabolites, and immune system, are also involved in the pathogenesis and development of NAFLD. Hepatic macrophage activation is induced by the permeation of antigens, endotoxins, and other proinflammatory substances into the bloodstream as a result of increased intestinal permeability. Therefore, it is important to understand the role of the gut–liver axis in influencing macrophage activity, which is central to the pathogenesis of NAFLD and nonalcoholic steatohepatitis (NASH). Not only probiotics but also biogenics (heat-killed lactic acid bacteria) are effective in ameliorating the progression of NASH. Here we review the effect of hepatic macrophages/Kupffer cells, other immune cells, intestinal permeability, and immunity on NAFLD and NASH and the impact of probiotics, prebiotics, and biogenesis on those diseases.     

The intestinal mucosa as a target for dietary polyunsaturated fatty acids

Several studies have reported beneficial effects of dietary polyunsaturated fatty acids (PUFA) on various aspects of both human and animal health, and particular reference has been made to their effects on systemic immune responses. Both immune stimulation and immune suppression have been reported, with the outcome dependent on the type of PUFA, the target cell, as well as the immune competence of the cells before exposure. The systemic and the mucosal immune systems are discrete entities, which have evolved specific approaches in the defense of the host. The latter comprises several interconnected tissues, which communicate with one another through the action of soluble mediators and the trafficking of cellular components. After the oral mucosa, the intestinal epithelium and its associated gutassociated lymphoid tissue are the primary targets of dietary components. Absorption of dietary PUFA and its incorporation into intestinal tissues has been well studied, but the consequences of these events in relation to local immune responses have received little attention. This article describes some of the immune mechanisms operating at this barrier and, where possible, pinpoints areas for which a modulatory role for PUFA has already been demonstrated. Although not an exhaustive treatise of the subject, it is hoped that this review will foster research into the specific interaction between dietary PUFA and cell populations comprising the intestinal barrier.     

Th17 Cells as Potential Probiotic Therapeutic Targets in Inflammatory Bowel Diseases

Inflammatory bowel diseases (IBD) are characterized by wasting and chronic intestinal inflammation triggered by various cytokine-mediated pathways. In recent years, it was shown that T helper 17 (Th17) cells are involved in the pathogenesis of IBD, which makes them an attractive therapeutic target. Th17 cells preferentially produce interleukin (IL)-17A–F as signature cytokines. The role of the interplay between host genetics and intestinal microbiota in the pathogenesis of IBD was demonstrated. Probiotics are live microorganisms that when orally ingested in adequate amounts, confer a health benefit to the host by modulating the enteric flora or by stimulating the local immune system. Several studies indicated the effectiveness of probiotics in preventing and treating IBD (ulcerative colitis, and Crohn’s disease). Furthermore, there is mounting evidence of probiotics selectively targeting the Th17 lineage in the prevention and management of inflammatory and autoimmune diseases such as IBD. This review highlights critical roles of Th17 cells in the pathogenesis of IBD and the rationale for using probiotics as a novel therapeutic approach for IBD through manipulation of Th17 cells. The potential molecular mechanisms by which probiotics modulate Th17 cells differentiation and production are also discussed.     

Overview of the Importance of Biotics in Gut Barrier Integrity

Increased gut permeability is suggested to be involved in the pathogenesis of a growing number of disorders. The altered intestinal barrier and the subsequent translocation of bacteria or bacterial products into the internal milieu of the human body induce the inflammatory state. Gut microbiota maintains intestinal epithelium integrity. Since dysbiosis contributes to increased gut permeability, the interventions that change the gut microbiota and correct dysbiosis are suggested to also restore intestinal barrier function. In this review, the current knowledge on the role of biotics (probiotics, prebiotics, synbiotics and postbiotics) in maintaining the intestinal barrier function is summarized. The potential outcome of the results from in vitro and animal studies is presented, and the need for further well-designed randomized clinical trials is highlighted. Moreover, we indicate the need to understand the mechanisms by which biotics regulate the function of the intestinal barrier. This review is concluded with the future direction and requirement of studies involving biotics and gut barrier.     

The Role of Leaky Gut in Nonalcoholic Fatty Liver Disease: A Novel Therapeutic Target

The liver directly accepts blood from the gut and is, therefore, exposed to intestinal bacteria. Recent studies have demonstrated a relationship between gut bacteria and nonalcoholic fatty liver disease (NAFLD). Approximately 10–20% of NAFLD patients develop nonalcoholic steatohepatitis (NASH), and endotoxins produced by Gram-negative bacilli may be involved in NAFLD pathogenesis. NAFLD hyperendotoxicemia has intestinal and hepatic factors. The intestinal factors include impaired intestinal barrier function (leaky gut syndrome) and dysbiosis due to increased abundance of ethanol-producing bacteria, which can change endogenous alcohol concentrations. The hepatic factors include hyperleptinemia, which is associated with an excessive response to endotoxins, leading to intrahepatic inflammation and fibrosis. Clinically, the relationship between gut bacteria and NAFLD has been targeted in some randomized controlled trials of probiotics and other agents, but the results have been inconsistent. A recent randomized, placebo-controlled study explored the utility of lubiprostone, a treatment for constipation, in restoring intestinal barrier function and improving the outcomes of NAFLD patients, marking a new phase in the development of novel therapies targeting the intestinal barrier. This review summarizes recent data from studies in animal models and randomized clinical trials on the role of the gut–liver axis in NAFLD pathogenesis and progression.     

Effects of Microbiota Imbalance in Anxiety and Eating Disorders: Probiotics as Novel Therapeutic Approaches

Anxiety and eating disorders produce a physiological imbalance that triggers alterations in the abundance and composition of gut microbiota. Moreover, the gut–brain axis can be altered by several factors such as diet, lifestyle, infections, and antibiotic treatment. Diet alterations generate gut dysbiosis, which affects immune system responses, inflammation mechanisms, the intestinal permeability, as well as the production of short chain fatty acids and neurotransmitters by gut microbiota, which are essential to the correct function of neurological processes. Recent studies indicated that patients with generalized anxiety or eating disorders (anorexia nervosa, bulimia nervosa, and binge-eating disorders) show a specific profile of gut microbiota, and this imbalance can be partially restored after a single or multi-strain probiotic supplementation. Following the PRISMA methodology, the current review addresses the main microbial signatures observed in patients with generalized anxiety and/or eating disorders as well as the importance of probiotics as a preventive or a therapeutic tool in these pathologies.     

Immune Cells in Cutaneous Wound Healing: A Review of Functional Data from Animal Models

The healing of skin wounds involves the activation and recruitment of various immune cell types, many of which are believed to contribute significantly to different aspects of the repair process. Roles for immune cells have been described in practically all stages of wound healing, including hemostasis, inflammation, proliferation and scar formation/remodeling. Over the last decade, tools to deplete immune cell populations in animal models have become more advanced, leading to a surge in the number of studies examining the function of specific immune cell types in skin repair. In this review, we will summarize what is known about distinct immune cell types in cutaneous wound healing, with an emphasis on data from animal studies in which specific cell types have been targeted.     

The Role of Gut Microbiota in an Ischemic Stroke

The intestinal microbiome, the largest reservoir of microorganisms in the human body, plays an important role in neurological development and aging as well as in brain disorders such as an ischemic stroke. Increasing knowledge about mediators and triggered pathways has contributed to a better understanding of the interaction between the gut-brain axis and the brain-gut axis. Intestinal bacteria produce neuroactive compounds and can modulate neuronal function, which affects behavior after an ischemic stroke. In addition, intestinal microorganisms affect host metabolism and immune status, which in turn affects the neuronal network in the ischemic brain. Here we discuss the latest results of animal and human research on two-way communication along the gut-brain axis in an ischemic stroke. Moreover, several reports have revealed the impact of an ischemic stroke on gut dysfunction and intestinal dysbiosis, highlighting the delicate play between the brain, intestines and microbiome after this acute brain injury. Despite our growing knowledge of intestinal microflora in shaping brain health, host metabolism, the immune system and disease progression, its therapeutic options in an ischemic stroke have not yet been fully utilized. This review shows the role of the gut microflora-brain axis in an ischemic stroke and assesses the potential role of intestinal microflora in the onset, progression and recovery post-stroke.