四种不同食性鱼类肠道微生物群落组成及多样性比较分析

本研究旨在探讨食性对鱼类肠道菌群组成和多样性的影响,并预测特定菌群对不同营养素的潜在功能。实验采用高通量16S rRNA基因测序技术,提取获得滇池高背鲫(Carassius auratus)、草鱼(Ctenopharyngodon idellus)、鳜鱼(Siniperca chuatsi)、昆明裂腹鱼(Shizothorax grahami) 4种不同食性鱼类的肠道内容物,12个样品的16S rRNA,构建文库并测序,分析这4种鱼类肠道微生物的菌落组成和多样性。结果显示,鱼类肠道菌群多样性受到食性的显著影响(P<0.05),综合表现为杂食性(滇池高倍鲫) > 草食性(草鱼) > 滤食性(昆明裂腹鱼) > 肉食性(鳜鱼)。4种鱼类具有一些相同的优势菌群：变形菌门(Proteobacteria)和厚壁菌门(Firmicutes)。然而,优势菌群在属水平上存在一定差异,如不动杆菌属(Acinetobacter)为鳜鱼的优势菌群,拟杆菌属(Bacteroides)为草鱼的优势菌群等。功能预测发现,鳜鱼肠道中以革兰氏阴性菌为主;草鱼抗病潜力略高于其他3种鱼类;约氏不动杆菌(A._ johnsonii)、鲁氏不动杆菌(A. lwoffii)和施氏假单胞菌(Pseudomonas stutzeri)可能有助于宿主对蛋白质的消化,而拟杆菌属中的某些菌群可能有助于宿主消化纤维素。综上所述,食性是影响鱼类肠道菌群组成和多样性差异化的主要因素之一,分析食性与肠道优势菌群之间的关联,探讨特异菌群的功能,可为研究鱼类营养代谢的微生物效应奠定理论基础。     

大豆凝集素对小肠上皮细胞和红细胞凝集能力的研究

本文旨在测定纯化的大豆凝集素对兔和鸡小肠上皮细胞和红细胞的凝集活性。测定大豆凝集素对红细胞的凝集能力时,采用2%兔红细胞悬液,测定了使兔红细胞50%凝集的蛋白质浓度。测定对兔小肠上皮细胞的凝集能力时,采用荧光标记SBA与新鲜小肠上皮细胞结合后,观察荧光显微镜下荧光结合细胞比例的方法定量。经血凝试验结果表明,使兔红细胞50%凝集的SBA蛋白质浓度为2.50~3.69μg/mL,而SBA对鸡的红细胞没有凝集作用。SBA对兔小肠上皮细胞有结合能力,结合率为30%左右。试验结果说明大豆凝集素的血凝活性具种属特异性,用SBA与小肠上皮细胞的结合率作为评价其抗营养活性的指标具一定可行性。     

内毒素对肠黏膜微血管内皮细胞内分泌一氧化氮和内皮素的影响

目的是研究内毒素（lipopolysaccharide; LPS）导致肠黏膜微血管内皮细胞损伤的作用机制。将所培养的肠黏膜微血管内皮细胞分为空白对照组和LPS组，每组按时间分为4个亚组：3h、6h、9h、12h。空白对照组加维持培养液，LPS组加1μg/ml LPS培养液，在CO2培养箱内静置培养。结果表明，一氧化氮（NO）分泌明显升高，3h后达到高峰，随后逐渐降低，而内皮素（endothelin; ET）分泌急剧升高，9h后达到高峰，随后又开始逐渐降低，但一直保持在较高的水平。所以引起了NO和ET的升高可能是LPS导致肠黏膜微血管内皮细胞的损伤机制。     

Effect of dietary vitamin B6 supplementation on growth and intestinal microflora of juvenile golden pompano (Trachinotus ovatus)

In order to investigate the dietary vitamin B₆ (VB₆) requirement for juvenile golden pompano, an experiment of six different diets with six dietary VB₆ levels (0, 3.75, 7.47, 10.6, 13.7 and 18.5 mg/kg) was conducted. The results indicated that the content of dietary VB₆ significantly increased weight gain rate (WGR), specific growth rate (SGR) and feed conversion ratio (FCR; p < 0.05). Golden pompano fed diet containing 7.47 mg/kg VB₆ achieved the maximum ALT, AST, GPx, hepatic VB₆ concentrations as well as the minimum MDA, however, the ALT, AST, GPx and hepatic VB₆ concentrations decreased while MDA increased with a further increase in dieatry VB₆. The highest values of GR and POD occurred at the 10.6 and 13.7 mg/kg dietary VB₆ (p < 0.05) respectively. A diet supplemented with 7.47 mg/kg VB₆ increased intestinal Na⁺, K⁺‐ATPase, Chymotrypsin, γ‐glutamyl transpeptidase, creatine kinase and amylase activities (p < 0.05). The relative abundance of Tenericutes and Bacteroidetes decreased while Proteobacteria and Firmicutes improved with an increase in dietary VB₆ levels up to 7.47 mg/kg. Quadratic regression analysis on WGR, hepatic VB₆ concentrations, AST and ALT indicated that the optimum dietary VB₆ levels for juvenile golden pompano were 8.84–9.28 mg/kg.     

不同脆化阶段草鱼肠道菌群动态变化、血清酶指标及生长性能

本研究旨在探讨草鱼(Ctenopharyngodon idellus)不同脆化阶段的肠道菌群组成结构、血清酶活性及生长性能,进而衡量脆肉鲩形成过程中的生理生化变化,以期为脆肉鲩的健康养殖提供科学数据.脆化不同阶段(30、60、90和120 d)的草鱼,在脆化结束后转投喂人工配合饲料30 d(第150天),鉴定整个过程中草鱼肠道菌群组成、血清酶活性和生长性能的变化.结果表明,60～150 d蚕豆组草鱼体重均低于对照组(P＜0.05,P＜0.01),90～120 d蚕豆组草鱼头肾体指数(head kidney somatic index,HKBI)和肝体指数(hepatosomatic index,HSI)均低于对照组(P＜0.05或P＜0.01),150 d时蚕豆组草鱼肝体指数与对照组无显著差异(P＞0.05);蚕豆组草鱼血清碱性磷酸酶、溶菌酶和补体C3(第30天除外)活性均低于对照组的,在转投喂饲料后,3种血清酶活性均出现回升趋势;与对照组相比,蚕豆组草鱼肠道菌群多样性降低,芽胞杆菌属(Bacillus)和鲸杆菌属(Cetobacterium)等有益菌数量减少,维氏气单胞菌(Aeromonas veronii)、温和气单胞菌(Aeromonas sobria)和鳗弧菌(Vibrio anguillarum)等条件致病菌数量增多.两组草鱼肠道核心菌群主要为变形菌门(Proteobacteria)、厚壁菌门(Firmicutes)、拟杆菌门(Bacteroidetes)和梭杆菌门(Fusobacteria).本研究结果提示,随着脆化时间的增加,摄食蚕豆改变草鱼肠道菌群组成、抑制血清酶活性和生长性能,在转投饲料后其肠道菌群、血清酶活性及生长性能均有所改善.本研究结果对脆肉鲩的健康养殖具有重要的科学指导意义.     

Heat stress-induced mucosal barrier dysfunction is potentially associated with gut microbiota dysbiosis in pigs

Heat stress(HS)can be detrimental to the gut health of swine.Many negative outcomes induced by HS are increasingly recognized as including modulation of intestinal microbiota.In turn,the intestinal microbiota is a unique ecosystem playing a critical role in mediating the host stress response.Therefore,we aimed to characterize gut microbiota of pigs’exposure to short-term HS,to explore a possible link between the intestinal microbiota and HS-related changes,including serum cytokines,oxidation status,and intestinal epithelial barrier function.Our findings showed that HS led to intestinal morphological and integrity changes(villus height,serum diamine oxidase[DAO],serum D-lactate and the relative expressions of tight junction proteins),reduction of serum cytokines(interleukin[IL]-8,IL-12,interferongamma[IFN-g]),and antioxidant activity(higher glutathione[GSH]and malondialdehyde[MDA]content,and lower superoxide dismutase[SOD]).Also,16S rRNA sequencing analysis revealed that although there was no difference in microbial a-diversity,some HS-associated composition differences were revealed in the ileum and cecum,which partly led to an imbalance in the production of short-chain fatty acids including propionate acid and valerate acid.Relevance networks revealed that HS-derived changes in bacterial genera and microbial metabolites,such as Chlamydia,Lactobacillus,Succinivibrio,Bifidobacterium,Lachnoclostridium,and propionic acid,were correlated with oxidative stress,intestinal barrier dysfunction,and inflammation in pigs.Collectively,our observations suggest that intestinal damage induced by HS is probably partly related to the gut microbiota dysbiosis,though the underlying mechanism remains to be fully elucidated.     

燕麦对肠道健康的保健价值

燕麦在改善肠道功能、预防便秘、调节肠道菌群以及防治肠道疾病等方面具有良好的功效.该研究从燕麦对肠道健康的方面进行重点阐述.     

紫锥菊多糖对LPS损伤后IEC-6分泌IL-6mRNA的影响

[目的]探讨紫锥菊多糖(EPS)在内毒素(LPS)损伤后IEC-6分泌IL-6mRNA的影响.[方法]采用Trizon试剂提取总RNA,经RT-PCR扩增后,进行琼脂糖凝胶电泳及图像分析.[结果]当LPS刺激IEC-6细胞时,IL-6mRNA分泌增加.而EPS可以抑制这种作用,并且具有剂量依赖性,50 μg/ml EPS可以部分抑制LPS刺激IEC-6产生的IL-6水平,而100、500μg/mlEPS随着浓度的增加,其抑制IL-6的水平逐渐增加;将IEC-6用50、100、200、500 μg/ml EPS预处理24h,然后用LPS(10 μg/ml)刺激1、4h,采用RT-PCR方法分析得,LPS诱导IL-6mRNA表达被EPS抑制且具有时间依赖性.[结论]证实了LPS作用于小肠上皮细胞后,其分泌的细胞因子IL-6mRNA产生增多,而EPS可以抑制LPS刺激细胞分泌的IL-6mRNA的产生从而起到肠道粘膜的保护作用,并且这种抑制作用具有浓度及时间依赖性.     

Host responses to Cryptosporidium infection

Cryptosporidium is a clinically and economically important infection whose pathogenic effect begins with colonization of the intestinal epithelium. Despite intensive efforts, a consistently effective therapy for the infection has yet to be identified. Morbidity and mortality results from ongoing loss of absorptive epithelium, which leads to villous atrophy and malabsorption and release of inflammatory mediators that stimulate electrolyte secretion and diarrhea. With further clarification of the mechanisms underlying enterocyte malfunction in Cryptosporidium infection, it should be possible to design rational nutritional and pharmacologic therapies to enhance nutrient and water absorption, promote the clearance of infected enterocytes, and restore normal villus architecture and mucosal barrier function.