激活素A对糖尿病肾脏病小鼠肾脏β-catenin信号通路调控的实验研究

目的:观察靶向调控激活素A(ACT A)下游β-连环蛋白(β-catenin)/T细胞因子(TCF)与β-catenin/叉头框转录因子-O(Foxo)信号的竞争抑制对糖尿病肾脏病(DKD)小鼠肾脏纤维化的影响。方法:30只小鼠随机将其分为对照组(A组)、糖尿病组(B组)、ACT A处理组(C组)、ACT A+iCRT3处理组(D组)和ACT A+iCRT3+AS1842856处理组(E组)。留取各组小鼠血、尿和肾组织样本,分别检测常规生化指标及肾脏病理改变,采用免疫组织化学法观察小鼠肾脏Ⅰ型胶原蛋白(CollagenⅠ)、N-钙黏蛋白(N-Cadherin)和波形蛋白(Vimentin)的表达。结果:与A组小鼠相比,B组小鼠肾脏指数(KW/BW)、尿微量白蛋白/肌酐比值(UACR)明显升高,肾组织Collagen I、N-cadherin和Vimentin的表达均增加;与B组小鼠比较,使用ACT A处理的C组小鼠的KW/BW、UACR及肾组织Collagen I、N-Cadherin和Vimentin的表达进一步上调;与C组相比,使用TCF阻断剂处理的D组小鼠KW/BW、UACR及肾...     

重组人Leptin对小鼠胃肠运动的影响

目的:观察重组人Leptin(rh-leptin)对小鼠胃肠推进运动的影响,并且探讨其作用机制.方法:经大肠杆菌重组表达并纯化获得rh-leptin.12只Km小鼠随机分为两组:rh-leptin组(n=6,腹腔注射rh-leptin 2.5 mg/kg)和对照组(n=6,腹腔注射生理盐水12.5 ml/kg),给药3 h后以5%的炭末阿拉伯胶混悬液灌胃,15 min后处死小鼠,比较两组小鼠炭末移动距离占小肠全长的百分率即小肠推进率,以观察rh-leptin对胃肠运动的影响.结果:对照组小肠推进率为(54.53±11.08)%,rh-leptin组小鼠肠推进率为(41.98±5.81)%,rh-leptin组小鼠小肠推进率显著降低(P＜0.05).结论:rh-leptin能降低小鼠胃肠蠕动速率,抑制其胃肠推进运动.     

白细胞介素-6和白细胞介素-10在不同细菌性血流感染小鼠模型中的表达及意义

目的:探讨白细胞介素(IL)-6和IL-10在不同病原菌所致细菌性血流感染中的表达及其意义.方法:建立金黄色葡萄球菌、粪肠球菌、大肠杆菌和肺炎克雷伯菌ICR小鼠血流感染模型,以注射相应剂量磷酸盐缓冲液的小鼠作为对照组,采用Luminex液相悬浮芯片系统检测各实验组和PBS对照组感染后0.5、1、3、6、12、24和48h时IL-6和IL-10的含量.结果:细菌感染小鼠后0.5 h时,各实验组IL-6的含量与对照组相比均明显升高(P＜0.05).各实验组IL-10的水平与对照组相比,感染后0.5h均明显升高(P＜0.05).大肠杆菌组、肺炎克雷伯菌组IL-10的含量在感染后1h达最大值.金黄色葡萄球菌组感染后3h达到最大值,粪肠球菌组在感染后6h达到最大值,且大肠杆菌组和肺炎克雷伯菌组IL-6和IL-10含量升高的幅度明显高于金黄色葡萄球菌组和粪肠球菌组(P＜0.05).对照组小鼠血清中IL-6和IL-10的含量在此过程中无明显变化.结论:IL-6和IL-10的含量在4种细菌性血流感染模型早期均明显升高.大肠杆菌组、肺炎克雷伯菌组IL-6和IL-10的含量升高幅度明显高于金黄色葡萄球菌组和粪肠球菌组.联合运用IL-6和IL-10有可能用于区分革兰阳性或革兰阴性细菌感染.     

急性肺损伤小鼠外周血树突状细胞数量及功能状态的变化

目的 探讨急性肺损伤(ALI)小鼠外周血树突状细胞(DC)数量及功能状态的变化.方法 雄性SPF级C57BL/6小鼠36只,6～8周龄,体重18～22 g,采用随机数字表法,将小鼠分为2组(n=18):对照组(C组)和ALI组.ALI组气管内注射脂多糖2 mg/kg,以制备ALI模型,C组注入等容量的PBS.于注入LPS或PBS后6、12和24 h(T1-T3)时随机取6只小鼠,麻醉后开胸取右心室血样,采用流式细胞仪检测外周血DC数量及DC表达CD80、MHCⅡ的水平;随后处死小鼠,取肺组织,计算湿重/体重(WW/BW)比,光镜下观察病理学结果,行肺损伤评分,采用ELISA法检测肺组织IL-6含量.结果ALI组可见肺泡间隔增宽、充血、出血及大量炎性细胞浸润等病理改变.与C组比较,ALI组各时点肺组织WW/BW比、IL-6含量、肺损伤评分升高,T1时外周血DC数量减少,T3时增多,T2、T3时DC表达MHCⅡ水平上调(P＜0.05).与T1时比较,ALI组T2时肺组织IL-6含量升高,T2、T3时外周血DC数量增多,DC表达MHCⅡ水平上调(P＜0.05);与T2时比较,ALI组T3时外周血DC数量增多(P＜0.05);2组各时点外周血DC表达CD80水平差异无统计学意义(P＞0.05).结论 ALI小鼠外周血DC数量早期减少,随后逐渐增多,功能呈渐成熟状态.     

外源性一氧化碳释放分子2对大肠杆菌活力及毒力的作用

目的 探讨外源性一氧化碳释放分子2(CORM-2)对大肠杆菌ATCC 25922菌株活力及毒力的作用及可能机制. 方法 (1)体外实验1.将菌株按照随机数字表法分为细菌组、细菌+1.2 mmol/L CORM-2组、细菌+1.6 mmol/L CORM-2组、细菌+1.2 mmol/L无活性CORM-2(iCORM-2)组、细菌+ 1.6 mmol/L iCORM-2组,每组样本数为6.细菌组不添加任何物质,其余4组添加相应浓度的CORM-2或iCORM-2.于培养0、3、5、8、10、12、16、20、24、27、30、48 h,测定各组菌液的增殖活性,结果以吸光度值(波长为600 nm)表示;同时进行菌落计数.(2)体外实验2.另取菌株,将其分为细菌组和细菌+0.8 mmol/L CORM-2组,采用基因芯片筛查出大肠杆菌的4个相关基因fliA、dnaK、marA和waaQ进行实时定量PCR(qRT-PCR),检测各基因表达量.(3)在体研究.另取菌株同体外实验1分组及处理,培养至细菌组菌液的吸光度值(波长600 nm)为0.4时,各组收集0.5 mL菌液.将72只C57BL/6小鼠按照随机数字表法分为空白对照组、细菌组、细菌+1.2 mmol/L CORM-2组、细菌+1.6 mmol/L CORM-2组、细菌+1.2 mmol/L iCORM-2组、细菌+1.6 mmol/L iCORM-2组,每组12只.空白对照组小鼠不行任何处理,其余5组小鼠取对应有或无添加物的0.5 mL菌液进行腹腔注射.注射后对后5组小鼠进行大体观察.注射后6、12 h检测后5组小鼠血清中TNF-α、IL-6水平,注射后12 h收集小鼠肝、肺组织标本检测髓过氧化物酶(MPO)活性.空白对照组小鼠行相同检测.对数据进行重复测量设计方差分析、析因设计方差分析、单因素方差分析和t检验. 结果 (1)体外实验1.与细菌组和细菌+ 1.2 mmol/L iCORM-2组比较,细菌+1.2 mmol/L CORM-2组多数时相点细菌增殖活性明显受抑,菌落明显数量减少(F值分别为1170.80、217.52,P值均小于0.01);与细菌组和细菌+ 1.6 mmol/L iCORM-2组比较,细菌+1.6 mmol/L CORM-2组多数时相点细菌增殖活性亦明显受抑,菌落数量亦明显减少(F值分别为7948.34、14 432.85,P值均小于0.01).(2)体外实验2.qRT-PCR检测结果显示:与细菌组比较,细菌+0.8 mmol/L CORM-2组fliA基因表达下调,dnaK、marA和waaQ基因表达上调(t值分别为30.28、-165.54、-168.88、-187.28,P值均小于0.01).(3)在体研究.细菌组和细菌+ 1.2 mmol/L iCORM-2组、细菌+1.6 mmol/L iCORM-2组小鼠出现诸如精神萎靡、呼吸急促等症状,细菌+ 1.2 mmol/L CORM-2组、细菌+1.6 mmol/L CORM-2组小鼠上述症状轻微或不明显.注射后6h,细菌组、细菌+1.2 mmol/L iCORM-2组小鼠血清TNF-α、IL-6水平分别为(647.3±3.8) pg/mL、(3.44±0.22) ng/mL以及(639.3±0.8)pg/mL、(2.47±0.32)ng/mL,明显高于细菌+ 1.2 mmol/L CORM-2组[(124.6±10.7) pg/mL、(1.03 ±0.16)ng/mL,t值为15.22～84.03,P值均小于0.01].与细菌组和细菌+1.6 mmol/L iCORM-2组比较,注射后6、12 h细菌+1.6 mmol/L CORM-2组小鼠血清TNF-α、IL-6水平亦均明显降低(t值为19.27～245.34,P值均小于0.01).注射后12 h,细菌+1.2 mmol/L CORM-2组小鼠肝、肺组织中MPO活性明显低于细菌组、细菌+ 1.2 mmol/L iCORM-2组,细菌+1.6 mmol/L CORM-2组小鼠肝、肺组织中MPO活性亦明显低于细菌组、细菌+ 1.6 mmol/L iCORM-2组(t值分别为17.36～18.92、2.35 ～3.61,P值均小于0.01).结论 CORM-2能够明显抑制大肠杆菌的活力和毒力,其抑制作用可能与其调节大肠杆菌部分重要的靶基因(fliA、dnaK、marA和waaQ)有关.     

机体能量代谢变化对腹腔镜袖状胃切除术后体重下降量的影响

目的:探讨机体能量代谢变化对腹腔镜袖状胃切除术后体重下降量的影响。方法:选择67例行腹腔镜袖状胃切除术的肥胖患者作为研究对象,术后6个月将其分为获得理想减重效果组,即多余体重减少百分比(%EWL)≥50%及未获得理想减重效果组(%EWL<50%)。对比分析术前及术后6个月能量代谢与体成分指标。结果:术后6个月,33例获得理想减重效果。相关性分析得出,%EWL与术后静息能量代谢(REE)/体重(BW)、△REE/BW、△去脂体重百分比呈正相关(r=0.473,P<0.001;r=0.372,P=0.002;r=0.493,P=0.003),%EWL与△呼吸商(RQ)、术后RQ呈现负相关(r=-0.613,P<0.001;r=-0.553,P<0.001)。多元逐步Logistic回归分析显示,术后REE/BW、RQ与获得理想减重效果密切相关。结论:术后REE/BW的增加及术后RQ的下降是获得理想减重效果的有效预测因子。     

菊苣酸对脓毒症相关性脑病小鼠认知功能的影响

目的 探讨菊苣酸对脓毒症相关性脑病(SAE)小鼠认知功能的影响.方法 健康雄性C57BL/6小鼠60只,6～8周龄,体重20～25 g.采用随机数字表法将小鼠分为四组:假手术组(S组)、脓毒症组(P组)、菊苣酸组(CA组)和菊苣酸+SIRT1抑制剂EX527组(CE组),每组15只.P组、CA组和CE组行盲肠结扎穿孔(...     

β防御素2与小鼠急性尿路感染的相关性

本文研究β防御素2(BD-2)与急性尿路感染的相关性。将18只BALB/c小鼠随机分为3组:正常组、尿路感染(UTI)模型组和阴性对照组,每组6只。正常组不做任何处理,UTI模型组采用大肠杆菌行UTI模型制备,阴性对照组采用等量的无菌0.9%氯化钠代替菌液。酶联免疫吸附测定法(ELISA)检测3组小鼠血液、尿液的BD-2浓度。HE染色观察3组小鼠泌尿系统(肾脏、膀胱和输尿管)的病理学炎症改变。实时定量PCR、免疫组化法评价BD-2在3组小鼠泌尿系统的表达。研究结果显示,UTI模型组小鼠的血液和尿液BD-2浓度明显高于正常组或阴性对照组(均P<0.05)。UTI模型小鼠的肾脏和膀胱炎症评分均要高于正常组(均P<0.05),而3组小鼠输尿管的炎症评分差异无统计学意义。3组小鼠BD-2 mRNA在泌尿系统的表达差异无统计学意义。BD-2蛋白在UTI模型小鼠肾脏和膀胱的表达均高于正常组或阴性对照组(均P<0.05),而3组输尿管中的BD-2表达差异无统计学意义。作者认为,急性UTI时小鼠血液和尿液中BD-2浓度明显升高,小鼠泌尿系统组织(肾脏、膀胱)中BD-2蛋白表达上升,预示BD-2可能参与了急性UTI的发病。     

微创压力超负荷小鼠心衰模型的建立

目的通过胸骨上窝途径微创建立小鼠心衰模型。方法选用雄性昆明种系小鼠,经胸骨上窝利用钽夹部分夹闭主动脉弓,通过测量心脏体重比(HW/BW)、心脏超声以及组织学检查观察该方法创建小鼠心衰模型可行性。结果部分夹闭主动脉弓10周,HW/BW较假手术组明显增加(P0.01);左室舒张期末直径(LVEDD)显著增大(P0.01);左室后壁舒张期末厚度(LVPWD)明显变薄(P0.01);射血分数(EF)以及短轴缩短率(FS)显著变小(P0.01);夹闭部分主动脉弓10周后其血清氨基末端B型利钠肽前体(NT-pro BNP)较假手术组明显增加(P0.01)。组织学观察左室部分心肌纤维排列紊乱、断裂,不同程度的结构破坏,心肌细胞呈不同程度变性及肥大,部分心肌细胞呈局灶性或片状坏死。结论经胸骨上窝途径部分夹闭主动脉弓建立小鼠心衰模型方法简单易行、微创、可靠。     

袖状胃切除术影响肥胖小鼠迷走神经传入神经元激素受体的表达

目的:探讨袖状胃切除术(SG)对迷走神经传入神经元(VANs)食欲相关激素受体表达水平的影响。方法:采用10周龄健康的小鼠给予高脂饮食喂养,获得12只饮食诱导肥胖(DIO)小鼠,采用随机数字表法随机分配至SG组和假手术配对组,每组6只。观察两组小鼠体质量和空腹血糖水平变化。6周后,无菌操作取出颈部迷走神经节,体外原代培...     

Role of bile in intestinal barrier function and its inhibitory effect on bacterial translocation in obstructive jaundice in rats

BACKGROUND: Our previous study using genetically labeled Escherichia coli strain JNW14 revealed that obstructive jaundice promotes bacterial translocation in rats and that the absence of bile in the intestinal tract is considered to be a factor inducing bacterial translocation. The aim of this study was to investigate the role of bile and bile acids in intestinal barrier function against bacterial translocation. MATERIALS AND METHODS: Eight-week-old male specific-pathogen-free Wistar rats were subjected to ligation of their common bile ducts (CBDL). The CBDL rats were treated with bacitracin, neomycin sulfate, and streptomycin sulfate, and the intestinal tract was colonized with E. coli strain JNW14, which was genetically labeled with resistant markers against the above three antibiotics, to monitor the bacterial translocation. The rats were then administered saline, cholic acid (20 mg/100 g BW), taurocholic acid (TCA: 5-50 mg/100 BW), or bile (1.5-6 mL/day) via a duodenal catheter. The degree of bacterial translocation of E. coli strain JNW14 to the mesenteric lymph nodes was compared. Histopathological examination of the terminal ileum and intestinal permeability test using phenolsulfonphthalein was also performed. RESULTS: Both cholic acid and TCA showed no inhibitory effect on bacterial translocation at any of the doses tested in CBDL rats, although TCA significantly decreased the numbers of E. coli strain JNW14 in the cecum. However, bile administration reduced the numbers of E. coli strain JNW14 in the cecum and mesenteric lymph nodes in CBDL rats although the inhibitory effect was weak. The integrity and permeability of the intestinal mucosa were kept at normal levels by bile administration in CBDL rats whereas the morphological changes, such as villous atrophy, villous edema, and lacteal canal dilatation, were observed in other CBDL rats. CONCLUSION: Bile plays an important role in maintaining the intestinal barrier function to prevent the invasion of enteric bacteria to the underlying tissues, suggesting that the intestinal administration of bile to patients with obstructive jaundice is a useful way to reduce infectious complications by inhibiting bacterial translocation from the intestine to other organs.     

肠道双歧杆菌与烫伤大鼠肠源性细菌/内毒素移位

目的　观察肠道双歧杆菌在肠源性细菌 /内毒素移位中的变化和作用。　方法　制作严重烫伤大鼠模型 ,同时设假伤组。检测细菌和内毒素 (LPS)移位及盲肠膜菌群变化 ,ELISA法检测血浆白细胞介素 6(IL 6)浓度。　结果　大鼠严重烫伤后脏器细菌移位明显增多 (P <0 .0 1) ;血LPS水平在致伤 1、3、5d后分别为 (0 .2 3 6± 0 148)Eu/ml、(0 .197± 0 .15 6)Eu/ml、(0 10 4± 0 .0 90 )Eu/ml,显著高于假伤组的 (0 .0 72± 0 .0 49)Eu/ml(P <0 .0 5 ) ;盲肠膜菌群中双歧杆菌数剧减 2 0～2 5 0倍、真菌数剧增至 5～ 60倍、大肠杆菌数增加 0 .5～ 3 0倍 ,双歧杆菌与大肠杆菌比值由假伤组的2 5 0 0 0∶1降为伤后的 4～ 80 0∶1;血浆IL 6水平显著增高。经分层统计 ,与未发生肠道细菌移位大鼠相比 ,盲肠膜菌群移位大鼠的双歧杆菌量减少约 12 0倍 ,真菌数增加约 5 0倍 ,大肠杆菌数增加约 3 0倍。盲肠膜菌群中双歧杆菌数量与血浆中IL 6、LPS浓度呈负相关 (r1=- 0 .4817,r2 =- 0 .4912 ,P <0 .0 1) ,血IL 6和LPS浓度间存在显著正相关 (r =0 .82 5 8,P =0 .0 0 0 1)。　结论　严重烫伤可导致大鼠盲肠膜菌群紊乱 ,细菌和LPS移位增加 ;盲肠膜菌群中双歧杆菌的比例和数量的减少 ,可能促使了严重烫伤后肠源性细菌 /内毒素移位     

Role of intestinal bifidobacteria in the pathogenesis of gut-derived bacteria/endotoxin translocation and the effect of bifidobacterial supplement on gut barrier function following burns

Early multiple organ dysfunction syndrome appears to be facilitated with bacterial translocation in severely burn injury, yet the mechanisms of bacterial translocation remains in dispute. The aim of this study was to investigate the potential role of intestinal bifidobacteria in the pathogenesis of gut-derived bacteria/endotoxin translocation following burns and the effects of bifidobacterial supplement on gut barrier. Methods: Wistar rats were randomly divided into burn group (Burn, n=60),sham burn group (SB, n=10) in experiment Ⅰ , and burn + saline group (BS, n=30), burn + bifidobacteria group (BB, n=30), and sham-burn + saline group (SS, n= 10) in experiment Ⅱ. Animals in BB group were fed bifidobacterial preparation (5 × 109 CFU/ml) after burns, 1.5ml,twice daily. Animals in BS and SS were fed saline. Samples were taken on days 1, 3, and 5 in burn groups, and on day 3 in sham-burn groups. The incidence of bacteria/endotoxin translocation and counts of Bifidobacterium, Fungi and Escherichia coli in gut mucosa were determined with standard methods. The levels of sIgA in mucus of small intestine were measured by RIA. The positive sIgA expression in lamina propria and ileum mucosal injury was evaluated light microscopically by blinded examiners. Results: Our results showed that the incidence of bacterial translocation was increased after burns, which was accompanied by significant decrease in number of bifidobacteria but significant increase in E. coli and fungi in gut mucosa, and elevation of levels of plasma endotoxin and IL-6 (P<0. 001).The incidence of bacterial translocation was markedly reduced after 3- and 5-day supplementation of bifidobacteria compared with control group (P<0.05). The counts of mucosal bifidobacteria were increased by 4- to 40-fold,while E. coli and fungi were decreased by 2- to 30-fold and 10- to 150-fold, respectively, after bifidobacterial supplementation in contrast to control group. The damage of mucosa tended to be less pronounced after 3-day bifidobacteria-supplemented formula compared with control group [grade 2(0-6) vs. grade 4(3-6), P<0.05]. Moreover, the expression and release of sIgA was markedly augmented after 3-day bifidobacteria-supplementation formula and it returned to normal range on day 5. Conclusion: The decrease in counts and proportion of bifidobacteria in mucous membrane flora may play an important role in the development of bacteria/endotoxin translocation following thermal injury. The supplement of exogenous bifidobacteria could per se improve gut barriers, and attenuate bacteria/endotoxin translocation secondary to major burns.     

The role of bifidobacteria in gut barrier function after thermal injury in rats

BACKGROUND: Early multiple organ dysfunction syndrome appears to be facilitated with bacterial translocation in severe burn injury, yet the mechanisms of bacterial translocation remain in dispute. The aim of this study was to characterize the potential role of intestinal bifidobacteria in the pathogenesis of gut-derived bacterial translocation after burns and to analyze the effects of bifidobacterial supplement on gut barrier function. METHODS: Wistar rats were randomly divided into burn group (Burn, n = 60), sham burn group (SB, n = 10) in experiment 1, and burn + saline group (BS, n = 30), burn + bifidobacteria group (BB, n = 30), and sham-burn + saline group (SS, n = 30) in experiment 2. Animals in BB group were fed bifidobacterial preparation (5 x 10(9) CFU/mL) after burns, 1.5 mL, twice daily. Animals in BS and SS were fed saline. Samples were taken on postburn days 1, 3, and 5. The incidence of bacterial translocation and counts of Bifidobacterium, fungi and Escherichia coli in gut mucosa, as well as the sIgA levels in mucus of the small intestine were determined. The positive sIgA expression in lamina propria and ileum mucosal injury were evaluated light microscopically by blinded examiners. RESULTS: The incidence of bacterial translocation was increased after burns, which was accompanied by significant decrease in number of bifidobacteria but significant increase in E. coli and fungi in gut mucosa, and elevation of levels of plasma endotoxin and IL-6 (p < 0.001). The incidence of bacterial translocation was markedly reduced after 3- and 5-day supplementation of bifidobacteria compared with control group (p < 0.05). The counts of mucosal bifidobacteria were increased by 4- to 40-fold, whereas E. coli and fungi were decreased by 2- to 30-fold and 10- to 150-fold, respectively, after bifidobacterial supplementation. The damage of mucosa tended to be less pronounced after 3-day bifidobacteria-supplemented formula compared with control group (grade 2 [0-6] versus grade 4 [3-6], p < 0.05). Moreover, the expression and release of sIgA was markedly augmented after 3-days of bifidobacteria-supplementation formula and it returned to normal range on postburn day 5. CONCLUSIONS: The decrease in counts and proportion of bifidobacteria to other flora in gut may play an important role in the development of bacterial translocation after thermal injury. Supplementation of exogenous bifidobacteria could improve gut barrier function, and attenuate bacterial/endotoxin translocation secondary to major burns.     

Role of bacterial adherence and the mucus barrier on bacterial translocation: effects of protein malnutrition and endotoxin in rats.

OBJECTIVE: The purpose of the study was to investigate the potential relations between mucosal bacterial adherence, intestinal mucus and mucin content, and bacterial translocation. SUMMARY BACKGROUND DATA: The attachment of bacteria to mucosal surfaces is the initial event in the pathogenesis of most bacterial infections that originate at mucosal surfaces, such as the gut. The intestinal mucus layer appears to function as a defensive barrier limiting micro-organisms present in the intestinal lumen from colonizing enterocytes. Consequently, studies focusing on the biology of bacterial adherence to the intestinal mucosa likely are to be important in clarifying the pathogenesis of gut origin sepsis. METHODS: To explore the relations between intestinal bacterial adherence, mucus bacterial binding, and bacterial translocation, two models were used. One (protein malnutrition) in which profound alterations in intestinal morphology occurs in the absence of significant translocation and one (endotoxin challenge) in which bacterial translocation occurs and intestinal morphology is relatively normal. RESULTS: Protein malnutrition was not associated with bacterial translocation and measurement of enteroadherent, mucosally associated bacterial population levels documented that the total number of gram-negative enteric bacilli adherent to the ileum and cecum was less in the protein-malnourished rats than in the normally nourished animals (p < 0.01). Furthermore, there was an inverse relation between the duration of protein malnutrition and bacterial adherence to the intestinal mucosa (r = 0.62, p < 0.002). In contrast, after endotoxin challenge, the level of enteroadherent bacteria was increased and bacterial translocation was observed. The binding of Escherichia coli to immobilized ileal mucus in vitro was decreased significantly in protein-malnourished rats, whereas E. coli binding to insoluble ileal mucus was increased in the rats receiving endotoxin. CONCLUSIONS: This study indicates that the adherence of bacteria to the intestinal mucosal surface is an important factor in bacterial translocation, that intestinal mucus modulates bacterial adherence, and that increased levels of mucosally associated bacteria are associated with a loss intestinal barrier function to bacteria.     

The effect of E coli virulence on bacterial translocation and systemic sepsis in the neonatal rabbit model

In the surgical neonate, three factors that promote bacterial translocation and systemic infection are: (1) intestinal bacterial colonization and overgrowth; (2) compromised host defenses; and (3) disruption of the mucosal epithelial barrier. The newborn rabbit provides an excellent model to study these factors. Like the human, there is early closure of the gut mucosa to macromolecules, and nutrition can be maintained by breast or formula feeding. This study examines translocation and systemic sepsis after colonization with virulent K1 and avirulent K100 strains of Escherichia coli. New Zealand white rabbit pups (2 to 5 days old) were studied. The gastrointestinal tracts of 12 were colonized with K1 E coli; 14 were colonized with K100 E coli; 12 control animals were not inoculated. Mesenteric lymph node (MLN), liver, spleen, and colon homogenate were cultured 72 hours postinoculation. No bacteria were isolated from the colons of all but one control animal. Translocation or systemic sepsis did not occur. Translocation to the MLN was significantly increased (P less than .03) in K1 (50%) and K100 (36%) groups compared with controls (0%). Translocation to liver and spleen (systemic sepsis) was significantly increased (P less than .03) in K1 animals (67%) compared with K100 (0%) or controls (0%). Colonization by both strains of E coli led to translocation to the MLN, but only K1 E coli caused systemic sepsis. This suggests that although colonization by E coli in the newborn leads to translocation to the MLN, progression to systemic sepsis is the result of characteristics of the bacteria and/or neonatal host responses.     

The effect of surgical trauma on the bacterial translocation from the gut.

Bacterial translocation is the passage of viable bacteria from the lumen of the gastrointestinal tract through the intestinal mucosa to other sites. It is believed that bacterial translocation may lead to infection and septicemia. The purpose of this study was to determine what factors in experimental surgical trauma lead to bacterial translocation. Two-month-old Wistar albino rats were divided into five groups: (A) control; (B) anesthesia (ether inhalation); (C) anesthesia and surgery (median laparotomy and transient compression of the intestines); (D) fasting only; and (E) anesthesia, surgery, and fasting. After 48 hours, ileum, mesenteric lymph nodes, and blood were cultured for aerobic and anaerobic organisms. In each group the number of animals with bacteria overgrowth was calculated. The incidence of bacterial translocation to mesenteric lymph nodes and blood in groups B and D were similar to the controls (P greater than .01). There was a significant increase in the number of animals with bacterial translocation in groups C and E (P less than .001). The majority of translocating bacteria were E coli.     

氯化镧对烫伤鼠肠道细菌移位的防治研究

目的　探讨氯化镧对烫伤鼠肠道细菌移位的作用及其机制。　方法　SD大鼠分为正常对照组 (A)、烧伤对照组 (B)及烧伤治疗组 (C) ,每组 30只。采用PUC19质粒转染大肠杆菌示踪加限制性内切酶指纹图谱分析法 ,对肠道菌向肠系膜淋巴结 (MLN)及血液中的播散进行示踪及定量研究。　结果　阳性菌落经酶切图谱分析后 ,证实B、C组MLN匀浆及血液培养生长细菌与灌胃的细菌具有完全相同的酶切图谱 ;C组MLN菌量在伤后 3、5d低于B组 (P <0 .0 5 )。C组血细菌阳性率在伤后 3d低于B组 (P <0 .0 5 )。C组血ET、NO及NOS量在伤后 1、3、5d均低于B组 (P <0 0 1)。C组肠组织MDA量在伤后 1、3、5d低于B组 (P <0 .0 1) ,C组肠组织SOD量在伤后 1、3d高于B组 (P<0 .0 5 )。　结论　血和MLN培养出的细菌由肠道细菌移位而来 ;氯化镧能有效防治肠道细菌移位 ;氯化镧通过抗菌、降低血中的ET、抑制NOS的活性减少NO的生成、提高SOD的活性并使MDA的产生下降等途径减少肠道细菌移位。     

表皮生长因子对重症胰腺炎肠外营养大鼠肠道细菌易位的影响

探讨表皮生长因子（ＥＧＦ）对重症胰腺炎（ＳＡＰ）全肠外营养（ＴＰＮ）支持大鼠肠道细菌易位的影响。方法：４８只ＳＤ大鼠随机分为ＳＡＰ组、ＳＡＰ＋ＴＰＮ组及ＳＡＰ＋ＴＰＮ＋ＥＧＦ组。分别测定肠系膜淋巴结、肝脏及脾脏细菌易位率,利用图像分析仪对小肠粘膜进行检测,并测定回肠粘膜厌氧菌与需氧菌的比率。结果：ＳＡＰ＋ＴＰＮ＋ＥＧＦ组肠系膜淋巴结、肝脏及脾脏细菌易位率明显降低,小肠粘膜绒毛面积、高度、隐窝深度增加,回肠厌氧菌与需氧菌的比率显著提高。结论：ＥＧＦ具有保护重症胰腺炎全肠外营养大鼠肠粘膜机械屏障、生物屏障和降低肠道细菌易位率的作用。     

益生菌与核黄素联用对烫伤大鼠肠道屏障的保护作用

目的　观察益生菌与核黄素联合应用对烫伤大鼠细菌移位的防治效果 ,探讨其可能的作用机制。　方法　将Wistar大鼠随机分为烫伤对照组 (SC组 ,30只 )、烫伤治疗组 (ST组 ,30只 )、正常对照组 (NC组 ,10只 )。SC、ST组大鼠作 30 %ⅢTBSA度烫伤 ,ST组大鼠伤后立即向胃中灌注含双歧杆菌 5× 10 12 个集落形成单位 /L、蜡样芽孢杆菌 5× 10 10 个集落形成单位 /L和核黄素 5 0 0mg/L的等渗盐水混悬液 1.5ml,2次 /d。SC、NC组于相同时间灌注等量等渗盐水。观察细菌移位、肠道膜菌群、回肠分泌型免疫球蛋白A(SIgA)合成分泌及肠黏膜损伤修复等变化。　 结果　与SC组比较 ,ST组大鼠各脏器细菌移位率显著下降 (P =0.0 0 0～ 0.0 2 5),血浆内毒素水平在伤后 3d内降低显著 (P <0 0 5 ),回盲部膜菌群中双歧杆菌量升高 2 0～ 4 0倍 ,大肠杆菌和真菌量显著降低 ( P <0.0 1),致伤后 5d内黏膜损伤评分为 0～ 3(P <0.0 5),小肠黏液SIgA含量伤后 5d可恢复正常 ( P <0 0 1)。结论　益生菌与核黄素联合应用 ,可减轻烫伤大鼠细菌 /内毒素移位程度 ,有效保护肠道屏障