Promotion of bacterial translocation by major liver resection in obstructive jaundice in rats colonised predominantly with indigenous Escherichia coli.
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The influence of major liver resection in obstructive jaundice on bacterial translocation was evaluated in rats that were colonised predominantly with a genetically labelled strain of Escherichia coli. The strain, JNW14, originally isolated from rat faeces, was labelled with bacitracin, neomycin and streptomycin resistance markers. Fifty-two specific-pathogen-free male Wistar rats were divided into three experimental groups and were treated as follows: group 1 (n = 8), sham ligation of common bile duct; group 2 (n = 7), common bile duct ligation (CBDL); and group 3 (n = 37), 70% hepatectomy 7 days after CBDL. The rats were treated with the above antibiotics and then given E. coli strain JNW14 in their drinking water. Translocation of E. coli JNW14 from the gastrointestinal tract to the mesenteric lymph nodes (MLNs), lungs, liver, spleen and portal vein was evaluated in each group. In group 3 (CBDL plus hepatectomy), the incidence of translocation of E. coli JNW14 to the liver and spleen after hepatectomy was significantly higher than in groups 1 and 2. This result indicates that major liver resection in obstructive jaundice promotes bacterial translocation to systemic organs. Furthermore, the numbers of viable E. coli JNW14 in the MLNs in the lung culture-positive rats were significantly higher than those in the lung culture-negative rats, suggesting that lymphatic-thoracic duct systemic circulation is a major route of bacterial translocation. (+info)
Microscopy of bacterial translocation during small bowel obstruction and ischemia in vivo--a new animal model.
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BACKGROUND: Existing animal models provide only indirect information about the pathogenesis of infections caused by indigenous gastrointestinal microflora and the kinetics of bacterial translocation. The aim of this study was to develop a novel animal model to assess bacterial translocation and intestinal barrier function in vivo. METHODS: In anaesthetized male Wistar rats, 0.5 ml of a suspension of green fluorescent protein-transfected E. coli was administered by intraluminal injection in a model of small bowel obstruction. Animals were randomly subjected to non-ischemic or ischemic bowel obstruction. Ischemia was induced by selective clamping of the terminal mesenteric vessels feeding the obstructed bowel loop. Time intervals necessary for translocation of E. coli into the submucosal stroma and the muscularis propria was assessed using intravital microscopy. RESULTS: Bacterial translocation into the submucosa and muscularis propria took a mean of 36 +/- 8 min and 80 +/- 10 min, respectively, in small bowel obstruction. Intestinal ischemia significantly accelerated bacterial translocation into the submucosa (11 +/- 5 min, p < 0.0001) and muscularis (66 +/- 7 min; p = 0.004). Green fluorescent protein-transfected E. coli were visible in frozen sections of small bowel, mesentery, liver and spleen taken two hours after E. coli administration. CONCLUSIONS: Intravital microscopy of fluorescent bacteria is a novel approach to study bacterial translocation in vivo. We have applied this technique to define minimal bacterial transit time as a functional parameter of intestinal barrier function. (+info)
Induction of intestinal inflammation in mouse by activation of proteinase-activated receptor-2.
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Proteinase-activated receptor (PAR)-2, a G-protein-coupled receptor for trypsin and mast cell tryptase, is highly expressed in the intestine. Luminal trypsin and tryptase are elevated in the colon of inflammatory bowel disease patients. We hypothesized that luminal proteinases activate PAR-2 and induce colonic inflammation. Mice received intracolonically PAR-2 agonists (trypsin, tryptase, and a selective PAR-2-activating peptide) or control drugs (boiled enzymes, inactive peptide) and inflammatory parameters were followed at various times after this treatment. Colonic administration of PAR-2 agonists up-regulated PAR-2 expression and induced an inflammatory reaction characterized by granulocyte infiltration, increased wall thickness, tissue damage, and elevated T-helper cell type 1 cytokine. The inflammation was maximal between 4 and 6 hours and was resolved 48 hours after the intracolonic administration. PAR-2 activation also increased paracellular permeability of the colon and induced bacterial trans-location into peritoneal organs. These proinflammatory and pathophysiological changes observed in wild-type mice were not detected in PAR-2-deficient mice. Luminal proteinases activate PAR-2 in the mouse colon to induce inflammation and disrupt the integrity of the intestinal barrier. Because trypsin and tryptase are found at high levels in the colon lumen of patients with Crohn's disease or ulcerative colitis, our data may bear directly on the pathophysiology of human inflammatory bowel diseases. (+info)
A prospective randomised study of the probiotic Lactobacillus plantarum 299V on indices of gut barrier function in elective surgical patients.
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BACKGROUND: Bacterial translocation occurs in surgical patients and may predispose to postoperative septic morbidity. Many factors are thought to influence the prevalence of bacterial translocation, one of which is the composition of the gut microflora. The aim of this prospective and randomised study was to assess the effect of the probiotic Lactobacillus plantarum 299v on the incidence of bacterial translocation, gastric colonisation, and septic complications in elective surgical patients. METHODS: Patients undergoing elective major abdominal surgery were randomised to either a treatment or control group. The treatment group received an oral preparation containing Lactobacillus plantarum 299v (Proviva) for at least one week preoperatively and also in the postoperative period. Bacterial translocation was determined by culture of a mesenteric lymph node and serosal scraping obtained at laparotomy. Gastric colonisation was assessed by microbiological culture of nasogastric aspirates. All postoperative septic complications were recorded. RESULTS: A total of 129 patients completed the study (probiotic group n=64). There was no significant difference between the two groups in terms of bacterial translocation (12% v 12%; p=0.82), gastric colonisation with enteric organisms (11% v 17%; p=0.42), or septic morbidity (13% v 15%; p=0.74). CONCLUSIONS: Administration of Lactobacillus plantarum 299v in elective surgical patients does not influence the rate of bacterial translocation, gastric colonisation, or incidence of postoperative septic morbidity. (+info)
An investigation into the sensitivities of translocating bacteria to a prophylactic antibiotic regimen.
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INTRODUCTION: It is well established that bacterial translocation is associated with a significant increase in septic morbidity. The purpose of this study was to determine the antibiotic sensitivities of translocating bacteria on the basis that this information may influence antibiotic prophylaxis in surgical patients. METHODS: Routine microbiological techniques were used to assess the antibiotic sensitivities of those bacteria cultured from a mesenteric lymph node harvested at laparotomy in a large series of patients. RESULTS: Culture of the mesenteric lymph nodes yielded growth in 51 out of a total of 447 patients studied (11.4%). The isolates from 40 patients, a total of 60 organisms, were available for sensitivity testing. The most common species grown was Escherichia coli (48% of isolates). Thirty-three patients (83%) grew organisms sensitive to the antibiotic prophylaxis used, but there was no significant difference in the incidence of postoperative septic complications between these patients and those in whom resistant bacteria were grown (39% versus 29%, P = 0.64 Fisher's Exact test mid P). CONCLUSIONS: The majority of translocating bacteria are sensitive to the prophylactic antibiotics commonly used in patients undergoing laparotomy. However, the occurrence of postoperative septic morbidity is independent of this variable. (+info)
Effects of interleukin-1alpha administration on intestinal ischemia and reperfusion injury, mucosal permeability, and bacterial translocation in burn and sepsis.
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OBJECTIVE: To evaluate the effect of interleukin-1alpha (IL-1alpha) on the mesenteric circulation, intestinal mucosal integrity, and bacterial translocation in a burn/endotoxemia chronic porcine model. SUMMARY BACKGROUND DATA: Major burn and sepsis are associated with a high mortality, ischemia/reperfusion injury to the intestine, and an increased rate of bacterial translocation. Pathologic alterations of IL-1 synthesis, degradation, and binding to receptors have been reported. Manipulation of IL-1-mediated effects might be of therapeutic utility. METHODS: Twenty-one female pigs were instrumented with an ultrasonic flow probe on the superior mesenteric artery and a catheter into the superior mesenteric vein. After 5 days, all animals were anesthetized, and 14 received 40% total body surface area third-degree burn. IL-1alpha was administered intravenously at 1,000 ng/kg to seven pigs immediately after burn. Eighteen hours after burn, 100 microg/kg lipopolysaccharide (LPS) was administered intravenously. Systemic and splanchnic hemodynamics were measured and blood samples were drawn for blood gas analysis. Intestinal permeability was assessed every 6 hours by measuring the lactulose/mannitol (L/M) excretion ratio. At the end of the study (42 hours), tissue samples were harvested for bacteriologic cultures. RESULTS: Mesenteric blood flow was significantly decreased after burn and endotoxin. Administration of IL-1alpha significantly improved mesenteric blood flow postburn and post-LPS. Mesenteric oxygen supply and consumption showed a significant reduction after burn. In contrast, animals treated with IL-1alpha showed an increase in postburn mesenteric oxygen supply and consumption. LPS-induced mesenteric hypoxia was also ameliorated by IL-1alpha treatment. Intestinal permeability, as assessed by the L/M ratio, showed a 7- and 10-fold elevation after thermal injury and LPS, respectively. In contrast, IL-1alpha-treated animals showed an increase of only three- and fourfold in the L/M ratio, respectively. Bacterial translocation was significantly increased in the burn/endotoxin group. IL-1alpha significantly reduced the rates of bacterial translocation. CONCLUSIONS: IL-1alpha treatment attenuates mesenteric ischemia and reperfusion injury induced by thermal injury and endotoxemia by improving mesenteric blood flow and oxygenation. Subsequently, IL-1alpha reduces intestinal permeability and bacterial translocation after burn and sepsis. (+info)
Effects of octreotide acetate and Saccharomyces boulardii on bacterial translocation in an experimental intestinal loop obstruction model of rats.
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Intestinal obstruction (IO) induces bacterial translocation (BT) due to mucosal disruption, motility dysfunction, and increased intestinal volume, leading to bacterial overgrowth. This study was conducted to investigate the effects of octreotide acetate (OA) and Saccharomyces boulardii (SB) on the BT and intestinal integrity in an animal model of intestinal loop obstruction (LO). Forty adult male Sprague-Dawley rats (250-300 g) were randomized into 4 groups containing 10 rats each. Complete IO was created in the distal ileum of rats by a single 3-0 silk suture (LO). Group Sham: Sham (Laparotomy only was performed in this group); group LO: LO; group OA: LO plus OA (100 microg/kg, at 0, 12 hours of obstruction); group (SB): LO plus SB (800 mg/kg/day, via orogastric and preoperative for 3 days). After 24 hours, samples of mesenteric lymph nodes (MLN), liver, spleen and blood were obtained and cultured. The terminal ileum specimens were examined histopathologically. There were no BT in group Sham, but BT was noticed totally in 31 (77.5%) cultures in group LO. This rate was reduced to 30% (n = 12), 10% (n = 4) in the groups OA and SB respectively. Bacterial translocations of MLN and the liver in group LO were significantly higher than those of groups OA and SB. Bacterial translocations of the both spleen and blood in group LO were significantly higher than those of groups OA and SB. The mean bacterial counts, colony-forming units per gram tissue (cfu/g), in the MLN, liver and spleen of group LO were found significantly higher than those of groups OA and SB. The mean villus height in group OA was significantly higher than that of group LO and it in the group SB significantly higher than those of groups LO and OA. The present experimental study has demonstrated that OA and SB may have protective effects against BT in mechanical bowel obstruction and additionally SB preserves intestinal mucosal integrity. (+info)
Glutamine deprivation facilitates tumour necrosis factor induced bacterial translocation in Caco-2 cells by depletion of enterocyte fuel substrate.
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BACKGROUND AND AIMS: Factors that induce luminal bacteria to cross the intestinal epithelium following injury remain poorly defined. The aim of this study was to investigate the interaction between glutamine metabolism, energy supply, and inflammatory mediators in determining the translocation of non-pathogenic bacteria across cultured enterocytes. METHODS: The effect of tumour necrosis factor alpha (TNF-alpha) on translocation of Escherichia coli C25 across Caco-2 epithelial monolayers was studied in the presence of products and inhibitors of glutamine metabolism. Simultaneous measurements of transepithelial electrical resistance (TEER) and flux of lucifer yellow were used to assess effects on the paracellular pathway. Lactate dehydrogenase release was used to monitor enterocyte integrity. Imaging of monolayers in these experimental conditions was undertaken with transmission electron microscopy. RESULTS: Exposure to basolateral TNF-alpha (20 ng/ml) for six hours induced translocation of E coli across Caco-2 but only if accompanied by simultaneous glutamine depletion (p<0.01). Translocation was inhibited by addition of glutamine for two hours (p<0.01) but not by an isonitrogenous mixture of non-glutamine containing amino acids. Inhibition of glutamine conversion to alpha-ketoglutarate, but not blockade of glutathione or polyamine synthesis, also induced translocation in the presence of TNF-alpha. Manipulations that induced bacterial translocation were associated with a marked reduction in enterocyte ATP levels. No effect of these treatments on paracellular permeability or lactate dehydrogenase release was observed. Conditions in which translocation occurred were associated with the presence of bacteria within enterocyte vacuoles but not the paracellular space. CONCLUSIONS: In inflammatory conditions, the availability of glutamine as an enterocyte fuel substrate is essential for the preservation of a functional barrier to microorganisms. In conditions of acute glutamine depletion, cytokine mediated bacterial translocation appears to be primarily a transcellular process. (+info)