Absence of intestinal bile promotes bacterial translocation.

Previously, the authors documented that extrahepatic biliary obstruction promotes the systemic translocation of bacteria from the intestine to visceral tissues. The current experiments were performed to determine whether it was the absence of intestinal bile or the presence of biliary obstruction that promoted bacterial translocation. Four groups of rats were studied: 1) nonoperated controls (n = 20), sham common bile duct-ligated (n = 22), common bile duct-ligated (n = 25), and common bile duct-diverted (choledochovesical bypass) (n = 23). The sham-ligated group underwent laparotomy and manipulation of the portal region; whereas the ligated group had their common bile ducts ligated, while the choledochovesical group had a silastic tube placed from the common bile duct to the bladder. Seven days later, at death, the incidence of bacterial translocation was higher in the groups of rats subjected to common bile duct ligation (41%) or diversion (32%) than in the control (3%) or sham-ligated (5%) groups (P less than 0.05). Histologic sections of ileums of ligated and diverted animals both showed subepithelial edema. These findings suggest that it is primarily the absence of bile in the intestine that promotes mucosal injury and bacterial translocation and not biliary obstruction.     

Immunosuppression and intestinal bacterial overgrowth synergistically promote bacterial translocation

Gram-negative, enteric bacilli of the indigenous gastrointestinal tract microflora translocated primarily to the mesenteric lymph nodes in mice given either oral penicillin G sodium or clindamycin hydrochloride. These bacteria also translocated to the mesenteric lymph nodes in mice injected with cyclophosphamide or prednisone. However, in mice treated with the combination of an oral antibiotic plus an immunosuppressive drug, the translocating bacteria spread systemically to the peritoneal cavity. When the treatment with clindamycin and prednisone was extended to 12 days, the mice died of lethal sepsis beginning eight days after treatment. Thus, the combination of intestinal bacterial overgrowth and host immunosuppression synergistically promoted bacterial translocation from the gastrointestinal tract that resulted in lethal sepsis.     

Effect of starvation, malnutrition, and trauma on the gastrointestinal tract flora and bacterial translocation

We have previously shown, in an animal model, that viable indigenous bacteria will cross the intact gastrointestinal (GI) mucosa and spread systemically, a process termed bacterial translocation, if the normal bacterial ecology of the gut was sufficiently disrupted to allow bacterial overgrowth or if the animals were severely immunosuppressed. Starvation or protein malnutrition disrupts the normal indigenous GI tract microflora and impairs host antibacterial defenses. Consequently, we tested the effect of the combination of starvation or protein malnutrition plus burn trauma in promoting bacterial translocation from the GI tract. Bacterial translocation was measured by quantitatively culturing the mesenteric lymph nodes, spleens, livers, blood, and peritoneal cavities of normal or burned (30% of total body surface area) CD1 mice deprived of food for three days or fed a low-protein (0.03%) diet. The effect of starvation or protein malnutrition on the gut microflora was determined by quantitatively measuring the levels of bacteria present in the ceca. Both starvation and protein malnutrition increased the cecal levels of gram-negative enteric bacilli and decreased the levels of lactobacilli and strict anaerobes. Surprisingly, neither starvation nor protein malnutrition promoted bacterial translocation, even though these animals lost over 20% of their body weight and the ecology of the gut microflora was disrupted. In fact, the protein-malnourished animals exhibited lower incidences of bacterial translocation than normally nourished animals when both groups were monoassociated with Escherichia coli C-25 or monoassociated and burned. Thus, it appears that protein malnutrition does not promote bacterial translocation, even when combined with burn trauma.     

Thermal injury promotes bacterial translocation from the gastrointestinal tract in mice with impaired T-cell-mediated immunity

We have shown previously that after thermal trauma viable bacteria will cross the intact gastrointestinal mucosa (bacterial translocation) to invade the mesenteric lymph nodes and other organs if the normal indigenous microflora is disrupted, allowing bacterial overgrowth. To determine whether T-cell-mediated immunity (T-CMI) was important in preventing translocation after thermal injury in animals with an intact normal flora, conventional (+/+), athymic (nu/nu), and heterozygous (nu/+) mice receiving a 30% third-degree burn were killed at various intervals after burn and their organs cultured. Bacterial translocation did not occur in control or burned specific pathogen-free mice with intact T-CMI but did occur in athymic mice with deficient T-CMI. Both the incidence of positive organs and the numbers of translocated bacteria per gram of organ were increased after thermal injury. Bacterial overgrowth was not responsible for these findings, since the levels of cecal enteric bacteria were not different between the burned and nonburned groups. Since translocation occurred to a greater extent in athymic burned mice than control athymic mice, it appears that a thermal injury promotes translocation by impairing other host defense systems in addition to the T-CMI.     

Endotoxin induces bacterial translocation and increases xanthine oxidase activity

Previously, we documented that endotoxin induces bacterial translocation from the gut and that inhibition or inactivation of xanthine oxidase activity reduces endotoxin-induced bacterial translocation. Consequently, experiments were performed to correlate endotoxin-induced bacterial translocation with changes in intestinal mucosal structure and xanthine dehydrogenase and oxidase activity. Segments of the jejunum, ileum, cecum, proximal colon, distal colon, and liver were harvested from ICR mice 24 hr after IP administration of E. coli 0111:B4 endotoxin (0.1 mg). Xanthine dehydrogenase and oxidase activities were measured in these samples and correlated with intestinal morphology. Bacteria translocated from the intestines to extraintestinal organs in 70% of the mice receiving endotoxin, while the organs of control mice were sterile (p less than 0.01). Endotoxin injured primarily the ileal and cecal mucosa and increased ileal and hepatic xanthine dehydrogenase and cecal oxidase activities (p less than 0.05). These results suggest that xanthine oxidase-induced mucosal damage plays a role in endotoxin-induced bacterial translocation.     

Prostaglandin E1 maintains structural integrity of intestinal mucosa and prevents bacterial translocation during experimental obstructive jaundice.

The absence of bile in the gut lumen induces mucosal injury and promotes bacterial translocation (BT). Prostaglandin E (PGE) has a protective effect on the mucosal layer of the alimentary tract. We hypothesize that PGE1 may prevent BT by its beneficial action on the mucosa of the small bowel. Thirty Wistar albino rats were divided equally into 3 groups; Group 1 (control) underwent sham laparotomy, group 2 obstructive jaundice (OJ) and group 3 (OJ + PGE1) underwent common bile duct (CBD) ligation and transection. Groups 1 and 2 received; 1 mL normal saline and group 3 received 40 mg of the PGE1 analogue misoprostol dissolved in 1 mL normal saline administered by orogastric tube once daily. After 7 days, laparotomy and collection of samples for laboratory analyses were performed, including bacteriological analysis of intestine, mesenteric lymph nodes (MLNs), and blood, and histopathologic examination of intestinal mucosa to determine mucosal thickness and structural damage. Serum bilirubin and alkaline phosphatase levels confirmed OJ in all animals with CBD transection. The mucosal damage score was significantly reduced in jaundiced animals receiving PGE1 compared to jaundiced controls (2.15 +/- 0.74 vs 5.3 +/- 0.59; p < .00001) and mucosal thickness was greater (607 +/- 59.1 microm vs. 393 +/- 40.3 microm; p < .00001). The incidence of BT to MLNs decreased from 90% to 30% (p < .02) when jaundiced rats received PGE1. PGE1 treatment reduced the detection rate of viable enteric bacteria in the blood from 60% to 10% (p < .057). We conclude that administration of PGE1 provides protection against OJ-induced atrophy and damage of intestinal mucosa, and thereby prevents translocation of enteric bacteria to underlying tissues.     

Effects of somatostatin analogues and vitamin C on bacterial translocation in an experimental intestinal obstruction model of rats.

The passage of viable endogenous bacteria and their products across the intact intestinal mucosal barrier, disseminating to the mesenteric lymph nodes, peritoneal cavity, spleen, liver, and circulation, is defined as bacterial translocation. Intestinal obstruction induces bacterial translocation due to mucosal disruption, motility dysfunction, and increased intestinal volume, leading to bacterial overgrowth. In a rat model of intestinal obstruction, the effects of both high-dose vitamin C (350 microg/kg), an antioxidant agent known to have a cytoprotective effect in ischemia-reperfusion injury, and somatostatin (20 microg/kg), a gastrointestinal antisecretory agent, in preventing bacterial translocation were studied. Both intestinal and liver samples from the rats was observed, and it was found that the rate of bacterial translocation was 100% in the control group, and only 43% for the rats who were given intraperitoneal vitamin C and somatostatin. The difference was statistically significant. In conclusion, we are convinced that vitamin C and somatostatin analogues may have protective effects against bacterial translocation in mechanical bowel obstruction.     

Bacterial translocation from the gastrointestinal tract and endogenous infection induced by immunosuppression after burn

This study described the endogenous infections and bacterial translocation from GI tract caused by immunosuppression after burn. In the group of burned plus injected dexamethasone (DXM) (BIS, n = 31), the rate of enteric bacteria translocation was 67.4%, the rate of visceral abscess was 65.5%, much more higher than in the group of only DXM (IS, n = 15). The translocation of intestinal bacteria also was found in the group of only burned (BU 3/15) and control (ck, 1/23), but endogenous infection did not occur in both group. The bacteria cultured from the rat organs are mainly enteric bacilli and corynebacterium. It was assumed that the endogenous infection was originated from the conditions in which the micro-ecologic system of indigenous intestinal flora was disturbed, immunologic function was suppressed by the overlapped effect of burn and injection of DXM, the biological antagonism among the intestinal flora was attenuated, and the intestinal bacilli overgrew, passed through the epithelia of intestine into lymphatic vessel and mesenteric lymph nodes, then colonized and multiplied in other organs, resulting in endogenous infection.     

大鼠急性胰腺炎肠道细菌易位的实验研究

目的本实验是观察大鼠急性胰腺炎后经胃肠道给予庆大霉素或谷氨酰胺对肠道细菌易位的影响。方法结扎封闭群 Wistar 大鼠的胆管,制成急性胰腺炎模型。分假手术组、急性胰腺炎组、庆大霉素组和谷氨酰胺组4组,各组又分5个亚组,分别于术后24、48、72、96和144小时处死动物。无菌下取回盲部淋巴结、胰腺、脾、肝、门静脉血和盲肠内容做细菌培养、计数。胰腺和小肠组织做病理检查。结果表明大鼠急性胰腺炎发生后,肠系膜淋巴结细菌数和阳性率明显增高,与门静脉血比较有显著差异。庆大霉索组盲肠内容和肠系膜淋巴结的大肠杆菌数明显减少,革兰氏阳性菌明显增多。谷氨酰胺组盲肠内容和肠系膜淋巴结的细菌数均显著减少。结论大鼠急性胰腺炎发生后早期肠道细菌易位主要经肠系膜淋巴途径。经胃肠道给予谷氨酰胺可防止肠道内细菌易位,减少胰腺感染的发生。     

Bacterial overgrowth and intestinal atrophy in the etiology of gut barrier failure in the rat

Bacterial translocation occurs in animal models of shock, trauma, sepsis, and parenteral or elemental enteral alimentation. Bowel atrophy and cecal bacterial overgrowth have both been implicated in the pathophysiology of bacterial translocation in many of these models. To further define the etiology of bacterial translocation resulting from dietary manipulations, rats were fed a elemental/defined-formula diet (DFD) for 2 weeks ad libitum and then randomized to either intestinal decontamination with a nonabsorbable antibiotic (neomycin) or no antibiotic treatment. Neomycin treatment significantly (p less than 0.01) reduced the incidence of bacterial translocation after DFD, in association with a significant reduction in the number of cecal gram-negative bacteria. Neither loss of bowel mass after DFD nor bowel composition was affected by oral neomycin. Bacterial translocation after DFD would thus appear to be the result of cecal bacterial overgrowth rather than a loss of a physical intestinal barrier due to atrophy.     

Effects of prostaglandin E1 and E2 analogues on mucosal injury-induced, and on bacterial translocation promoted by, experimental intestinal obstruction.

The aim of this experimental study was to investigate effects of prostaglandin E1 and E2 analogues on mucosal structure and bacterial translocation during small bowel obstruction. The study was carried out on 40 Wistar rats equally divided into four groups; group 1 = control, group 2 = intestinal obstruction by ligation of distal ileum, and groups 3 and 4 = obstruction and administration of PGE2 and PGE1, respectively. Intestinal bacterial content and translocation to mesenteric lymph nodes and to the blood were determined by microbiological analysis. Mucosal structural changes were assessed by histopathological examination and expressed as a structural damage score and as the thickness of the mucosal layer. Bacterial overgrowth was determined in all obstruction groups. Mucosal thickness was 39.7 microm in group 1 and 26.8 microm in group 2 (p <.001). The thickness was significantly preserved by administration of PGE1 and PGE2 (p <.001). Mean structural damage score was 0.4 in group 1 and 6.7 in group 2 (p <.001). The damage scores were significantly lower in groups treated with PGE1 and PGE2 than obstruction alone group (p <.001). Better scores were obtained in rats treated with PGE1 than rats treated with PGE2 (p =.0026). Translocation to the lymph nodes did not occur in group 1, but was 70% in group 2 (p =.0015); significantly lower rates of translocation to lymph nodes were observed in rats treated with PGE1 (p =.035), but not with PGE2. We conclude that mucosal structure is partly maintained by administration of PGE1 and PGE2 during intestinal obstruction; PGE1 is more effective than PGE2 for ameliorating mucosal injury. PGE1 prevents bacterial translocation by preserving structural integrity of the mucosa. PGE2 partially prevents mucosal damage but not bacterial translocation.     

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.     

Endotoxin-induced bacterial translocation: a study of mechanisms

Previously, we documented that nonlethal doses of endotoxin cause the translocation (escape) of bacteria from the gut to systemic organs. The purpose of this study was to determine which portion(s) of the endotoxin molecule induces bacterial translocation and to examine the role of xanthine oxidase activity in the pathogenesis of endotoxin-induced bacterial translocation. Nonlethal doses of Salmonella endotoxin preparations (wild type, Ra, or Rb), containing the terminal portion of the core polysaccharide, induced bacterial translocation, whereas those preparations lacking the terminal-3 sugars (Rc, Rd, Re, or lipid A) did not induce bacterial translocation. Additionally, only those endotoxin preparations that induced bacterial translocation injured the gut mucosa, increased ileal xanthine dehydrogenase and oxidase activity, and disrupted the normal ecology of the gut flora, resulting in overgrowth with enteric bacilli. Inhibition of xanthine oxidase activity by allopurinol prevented endotoxin (Ra)-induced mucosal injury and reduced the incidence of bacterial translocation from 83% to 30% (p less than 0.01). These results suggest that endotoxin-induced bacterial translocation requires the presence of the terminal core lipopolysaccharide moiety and that xanthine oxidase-generated oxidants are important in the pathogenesis of endotoxin-induced mucosal injury and bacterial translocation.     

阻塞性黄疸大鼠肠黏膜屏障功能变化及力肽的治疗作用

目的探讨阻塞性黄疸大鼠肠黏膜屏障功能变化以及力肽的治疗作用。方法将36只Wistar大鼠随机分成胆管结扎组（BDL）、假性手术组（SL）、胆管结扎＋力肽治疗组（Dipeptiven）3组，分别于术后24h、72h、1周和2周测定血浆内毒素值（Endotoxin，ET），并于2周后作细菌移位率和肠黏膜组织学检查。结果BDL组厌氧菌移位阳性率（58．33％）及各时间点血浆ET值显著高于SL组（0）和Dipeptiven组（8．33％）（P〈0．01），Dipeptiven组在各时间点血浆ET值较BDL组显著降低（P〈0．01）。组织学检查显示，BDL组肠黏膜发生了实质性损害。结论阻塞性黄疸时肠黏膜屏障损害可能促进肠道细菌移位，导致感染易感性增高。而力肽可改善受损小肠黏膜结构及减轻肠道细菌移位。     

Internal biliary drainage improves decreased number of gut mucosal T lymphocytes and MAdCAM-1 expression in jaundiced rats

BACKGROUND: Although the effect of preoperative biliary drainage in patients with obstructive jaundice is controversial, bacterial or endotoxin translocation is one of the main postoperative problem in jaundiced patients. Failure in gut barrier functions causes bacterial translocation; homing and distribution of T lymphocytes in the intestinal lamina propria are important for gut mucosal immune defense. This study was performed to examine whether bile regulates the numbers of T lymphocyte subsets or the expression of mucosal addressin cell adhesion molecule-1 (MAdCAM-1) in experimental jaundice in rats with and without external and internal biliary drainage. METHODS: Four groups of Wistar rats were used: those that received a sham operation (SHAM), common bile duct ligation (CBDL), CBDL followed by external drainage (ED), and CBDL followed by internal drainage (ID). Numbers of CD4(+) and CD8(+) T lymphocytes and MAdCAM-1-positive cells in the lamina propria were counted immunohistochemically in the specimens of jejunum and ileum of each group. Bacterial translocation was examined by culturing from the mesenteric lymph node complex isolated from rats in each group. RESULTS: A significant decrease in numbers of CD4(+) and CD8(+) T lymphocytes and MAdCAM-1-positive cells in the lamina propria was seen in obstructive jaundice, although numbers of peripheral blood lymphocytes increased in comparison with the sham-operated control. The numbers of CD4(+) and CD8(+) T lymphocytes and MAdCAM-1 expression in the lamina propria did not recover to a normal level after external drainage, but did so after internal drainage. Frequencies of bacterial translocation were high in the CBDL and ED group. In contrast, bacterial translocation was not present in any animals in the SHAM group and was at a low percentage in the ID group. CONCLUSIONS: Changes in the number of T lymphocytes and MAdCAM-1 expression are associated with the presence of bile in the gastrointestinal tract and are inversely correlated with the frequency of bacterial translocation induced by CBD ligation. MAdCAM-1 expression maintained by the presence of bile may regulate T-lymphocyte homing to the lamina propria in obstructive jaundice.     

Hyperbaric oxygen prevents bacterial translocation in thermally injured rats.

This study was designed to evaluate the effects of hyperbaric oxygen (HBO2) on intestinal microflora and bacterial translocation (BT) caused by experimentally induced thermal injury in rats. Rats were separated into four groups, namely, HBO2 group, thermal injury (TI) group, TI + HBO2 group, and control group. All groups were further separated into short-term (2 days) and long-term (7 days) treatment or injury groups. Control group was neither exposed to thermal injury nor was given any treatment. Thirty percent second-degree thermal burn was induced on the dorsal body part of the rats in TI groups. In the HBO2 groups, rats received HBO2 treatment either without TI or following TI induction, for 2 and 7 days, respectively. Sampling from tissues and portal vein was performed on day 3 in the short-term groups and on day 8 in the long-term groups. Samples were cultured for identification of bacteria and colony counts. HBO2 treatment significantly reduced the colony counts of endogenous microflora in distal ileum of healthy rats (p < .05), while TI significantly increased the colony counts of endogenous microflora in distal ileum in short and long-term TI groups (p < .05). Presence of bacterial translocation was proven by bacterial isolation in mesenteric lymph nodes, liver, spleen and blood. Both short- and long-term HBO2 treatment following TI significantly reduced the colony counts of intestinal microflora (p < .05) and prevented bacterial translocation almost completely. It is concluded that thermal injury causes both bacterial overgrowth within intestinal lumen and bacterial translocation across the intestinal wall. HBO2 administration prevents both bacterial overgrowth and translocation.     

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.     

Clostridium difficile toxins and enterococcal translocation in vivo and in vitro

BACKGROUND: Clostridium difficile toxins alter permeability in cultured enterocytes and may alter intestinal epithelial permeability to bacteria in vivo. Experiments were designed to test the effects of C. difficile toxins on in vitro interactions of Enterococcus gallinarum with cultured enterocytes, as well as on translocation of E. gallinarum in mice. MATERIALS AND METHODS: Mature Caco-2 and HT-29 enterocytes were pretreated with C. difficile toxin A or toxin B followed by incubation with E. gallinarum. E. gallinarum-enterocyte interactions were assessed by quantitative culture. For in vivo experiments, antibiotic-treated mice were orally inoculated with C. difficile or saline, and all mice were orally inoculated 24 h later with E. gallinarum and sacrificed after another 24 h for analysis of cecal bacteria, cecal C. difficile toxin, and enterococcal translocation. Cecal C. difficile toxin was assayed as cytopathic effects on human foreskin fibroblasts. RESULTS: Although neither toxin had a noticeable effect on bacterial internalization by cultured enterocytes, C. difficile toxins were associated with increased E. gallinarum transmigration across confluent enterocyte cultures. Mice orally inoculated with saline rather than C. difficile (n = 29) had no detectable cecal toxin, while mice orally inoculated with C. difficile (n = 30) had detectable cecal toxin. Viable E. gallinarum was recovered from the mesenteric lymph nodes of 97% of mice orally inoculated with saline followed by oral E. gallinarum, but only 37% of mice orally inoculated with C. difficile followed by oral E. gallinarum (P < 0.01). CONCLUSIONS: These results suggested that observations with cultured enterocytes, demonstrating that C. difficile toxins facilitated bacterial migration across the intestinal epithelium, might have little in vivo relevance in a mouse model of antibiotic-induced C. difficile overgrowth.     

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.     

选择性肠道脱污染预防急性坏死性胰腺炎继发感染的实验研究

目的　通过急性坏死性胰腺炎(ANP)动物模型,探讨选择性消化道脱污染(SDD)预防胰腺继发感染的作用。方法　Wistar大鼠60只,向总胆胰管逆行输入人工胆汁复制ANP模型,随机设立正常对照组、假手术对照组、ANP组和SDD治疗组,观察胰肠组织学、胰淀粉酶、肠道菌群、脏器细菌移位率和死亡率的变化。结果　SDD使ANP动物胰腺和小肠粘膜病理改变减轻,胰淀粉酶水平下降(P＜0.05),并使ANP时肠道菌群的紊乱状态得以恢复,肠粘膜和肠内容物双歧杆菌/大肠杆菌比值(B/E)分别由-0.37±0.72升至1.73±1.23(P＜0.01)和由0.88±0.77升至无穷大。SDD组72h脏器细菌移位率由59.5%降至33.3%(P＜0.05),72h死亡率由58.8%降至14.3%(P=0.005)。结论　SDD通过减轻肠道菌群紊乱状态,减少细菌移位,有利于预防ANP继发感染。