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PubMed2004

[Effect of glutamine on the non-steroidal anti-inflammatory drug-induced bacterial translocation].

BACKGROUND/AIMS: NSAIDs induce gut damage throughout the entire gastrointestinal tract and bacterial translocation. The aim of this study was to examine if administration of glutamine was able to prevent the NSAID-induced gut damages and bacterial translocation in the animal models. METHODS: Rats were utilized into 5 groups; control group, diclofenac group, and diclofenac with glutamine 0.8, 1.6, and 3.2 g/kg/day group. The animals with glutamine were fed with L-glutamine for 4 days before diclofenac administration. Gut injury was induced by administration of a single dose of diclofenac (80 mg/kg orally). Intestinal permeability (24 hour urinary excretion of phenolsulfonphthalein), enteric aerobic bacterial counts, serum biochemical profiles and bacterial translocation to mesenteric lymph nodes, liver and spleen were measured. RESULTS: Diclofenac caused the increase in intestinal permeability, enteric bacterial count, enteric protein and albumin loss and bacterial translocation. Administration of glutamine reduced the increase in intestinal permeability, protein losing enteropathy, enteric bacterial overgrowth and bacterial translocation induced by diclofenac. CONCLUSIONS: Glutamine may have beneficial effects on NSAID-induced gut damage and bacterial translocation.

Animals↗
PubMed1987

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.

Animals↗
PubMed1991

Hemorrhagic shock and bacterial translocation in a swine model.

Bacterial translocation is proposed as an explanation for sepsis associated with hemorrhagic shock. This study attempted to document these events in a large animal model. Male swine were randomly assigned to control (n = 10) or experimental (n = 10) groups. Animals were anaesthetized, and the bladder, portal vein, and a mesenteric lymphatic vessel cannulated. Experimental animals were bled 40% of blood volume. Over the next six hours maintenance fluids were given, and cultures of portal blood and mesenteric lymph taken. Before the swine were killed, cultures were taken from portal and systemic blood, mesenteric lymph, and lymph nodes, and a portion of terminal ileum was resected for histologic study. Experimental animals experienced significant shock as demonstrated by changes in hemodynamic and biochemical variables. Cultures and histologic examination of the terminal ileum showed no significant difference between control and experimental animals. In an unresuscitated swine model, significant bacterial translocation was not demonstrated within six hours of hemorrhagic shock.

Animals↗
PubMedDate not supplied

Elemental diet-induced bacterial translocation associated with systemic and intestinal immune suppression.

BACKGROUND: Elemental diets can lead to a loss of intestinal barrier function, promote bacterial translocation, and impair host immune defenses. The purpose of this study was to determine the effects of i.v. and orally administered total parenteral nutrition (TPN) solution on systemic and intestinal immunity and to establish whether supplemental cellulose fiber could improve the impaired immune response. METHODS: The incidence of bacterial translocation and immune function was quantitated by measuring organ weights, immune cell population levels, and the mitogenic response of lymphocytes from the spleen, mesenteric lymph nodes and Peyer's patches of rats receiving parenteral or enteral TPN solution, with and without fiber supplementation. RESULTS: Parenteral and enterally administered TPN solution promoted bacterial translocation to the mesenteric lymph nodes, reduced immune cell population levels, and decreased the lymphocyte mitogenic response to T- and B-cell mitogens. Supplemental cellulose fiber reduced the incidence of diet-induced bacterial translocation from 84% to 31% (p < .01) and improved immune cell function. To more closely examine the relationship between bacterial translocation and impaired lymphocyte mitogenic activity, rats receiving TPN orally or i.v. were separated into two groups based on whether or not bacterial translocation occurred. Rats in which fiber prevented bacterial translocation had normal mitogenic responses, whereas the sub-group of rats in which fiber failed to prevent bacterial translocation had profound decreases in their lymphocyte mitogenic responses. CONCLUSIONS: Both parenteral and enteral elemental diets induced bacterial translocation and impaired systemic and intestinal immune function. Fiber supplementation was effective in reducing elemental diet-induced bacterial translocation and significantly prevented diet-induced impairment of lymphocyte function.

Administration, Oral↗
PubMed1996

The association of gut-associated lymphoid tissue and bacterial translocation in the newborn rabbit.

The authors have previously demonstrated spontaneous bacterial translocation (BT) in newborn rabbits and its resolution with aging. It is hypothesized that this spontaneous BT was associated with an immature gut-associated lymphoid tissue (GALT). The aim of the present study was to characterize the cellular populations of the GALT in rabbits at various ages and to correlate this with the frequency of BT. Small bowel (SB) sections and mesenteric lymph nodes (MLN) were harvested and cultured (aerobically) from New Zealand White rabbits at 0, 6, 14, 28, and more than 90 days of age for determination of bacterial colonization (BC) and BT. Portions of ileum (n = 6 for each age) were simultaneously harvested for immunoperoxidase staining. Total T cells (CDS+), expressed as the number of positive cells/1000 nuclei and activated T cells (CD25+), expressed as the number of positive cells/1000 nuclei and as the ratio of CD25+/CD5+ cells, were analyzed for each tissue. Positive cells were counted in 30 villi by light microscopy. The incidence of BT rose as BC increased in the small bowel and peaked at 6 days of age; BT then decreased with age. CD5+ cells in the small bowel villi at 0 days of age were few (2.5 positive cells/1000 nuclei) and the number significantly increased with age (6 days, 6.5; 14 days, 19.0; 28 days, 31.6; adult, 136.6 positive cells/1,000 nuclei). The distribution of T cells started in the crypts, and with advancing age, cells were found all the way to the top of the villi. The number of CD25+ cells in the villi increased with age. The CD25+/CD5+ ratio in the small bowel villi peaked at 6 days of age. These results demonstrate an inverse relationship between the number of CD5+ cells in the intestinal villi and the incidence of bacterial translocation. The elevation of activated T cells (CD25+) at 6 days of age may be the result of an immunologic activation during the time of peak bacterial translocation. These data suggest that maturity of the GALT leads to a loss of spontaneous bacterial translocation in the newborn period. Modalities that supplement the GALT may help reduce bacterial translocation.

Aging↗
PubMed2001

Hyperbaric oxygen prevents bacterial translocation in rats with obstructive jaundice.

This study was designed to demonstrate bacterial translocation following bile duct ligation and investigate preventive effects of hyperbaric oxygen on obstructive jaundice-related bacterial translocation in an animal model. Hyperbaric oxygen treatment significantly reduced the endogenous colony counts in distal ileum of normal rats both in the short (two days) and long (seven days) term. Endogenous bacteria in distal ileum significantly increased in bile duct ligated rats in the short and long term, and presence of bacterial translocation was proven by bacterial growth in mesenteric lymph nodes, liver, spleen, and blood. Short- and long-term hyperbaric oxygen treatments significantly reduced the intestinal colony counts and prevented the bacterial translocation almost completely in rats with bile duct ligation. It is concluded that obstructive jaundice causes bacterial overgrowth and translocation, and hyperbaric oxygen treatment can prevent both bacterial overgrowth and translocation effectively.

Animals↗
PubMed1994

Bacterial translocation: nursing implications in the care of patients with neutropenia.

PURPOSE/OBJECTIVES: To describe bacterial translocation; the potential causes and influencing factors of bacterial translocation; the anatomy, physiology, and immunology of the small intestine; and the significance of bacterial translocation in patients with cancer. DATA SOURCES: Published articles and books, as well as clinical experience. DATA SYNTHESIS: 50% of infections in patients with cancer who are neutropenic result from endogenous sources such as the normal microbial flora of the bowel. This process called bacterial translocation may be responsible for symptoms such as fever of unknown origin in these patients. CONCLUSION: Maintaining normal bacterial ecology and mucosal integrity of the bowel can reduce the risk of bacterial translocation. IMPLICATIONS FOR NURSING PRACTICE: Care is directed at preventing constipation and maintaining integrity of the normal bowel and microbial flora by providing a low-microbial diet that contains adequate fluid and fiber and by encouraging good oral care.

Bacterial Physiological Phenomena↗
PubMed1994

Bombesin protects against bacterial translocation induced by three commercially available liquid enteral diets: a prospective, randomized, multigroup trial.

OBJECTIVE: To test the hypothesis that certain commercially available liquid diets would cause bacterial translocation and that this diet-induced translocation could be reduced with bombesin (an intestinal hormone stimulant). DESIGN: Prospective, multigroup trial in which animals fed each test diet were randomized to receive either bombesin or saline for 7 days. On day 7, the mice were killed and their organs were cultured for translocating bacteria, their cecal bacterial population concentrations were measured, and ileal and jejunal mucosal protein content was determined. SETTING: Small animal laboratory. SUBJECTS: Outbred ICR mice weighing 25 to 35 g. INTERVENTIONS: Mice received bombesin (10 micrograms/kg) or saline subcutaneously three times daily for 7 days before sacrifice. MEASUREMENTS AND MAIN RESULTS: The incidence of bacterial translocation to the mesenteric lymph node was significantly increased (p < .05) in mice fed Vivonex (53%), Criticare (67%), or Ensure (60%) compared with chow-fed controls (0%). All three liquid diets were associated with the development of cecal bacterial overgrowth and loss of jejunal and ileal mucosal protein content. Bombesin reduced the incidence of bacterial translocation and loss of mucosal protein content in all three liquid diet groups (p < .05), but did not prevent diet-induced cecal bacterial overgrowth. CONCLUSIONS: Three different liquid diets induced bacterial translocation to the mesenteric lymph node. Since bombesin was effective in reducing bacterial translocation, it appears that bacterial translocation induced by these liquid diets can be modulated hormonally.

Animals↗
PubMed2004

Probiotics partly reverse increased bacterial translocation after simultaneous liver resection and colonic anastomosis in rats.

BACKGROUND: Bacterial translocation is one important cause of nosocomial infections following major abdominal surgery. Oral administration of probiotics has been proposed to diminish bacterial translocation. MATERIAL AND METHODS: In total 68 rats were divided into seven groups: five of the groups received standard rat chow and were subjected to either sham-operation, 70% liver resection, colonic anastomosis, or a combination of 30 or 70% liver resection with synchronous colonic anastomosis, respectively. In two additional groups with synchronous operation, a combination of four different lactic acid bacteria and four fibers was administered two times daily pre- and postoperatively. Bacterial concentrations in cecum, mesenteric lymph nodes, liver, and spleen were analyzed and blood cultures were taken 48 h after operation. Furthermore, the following parameters were assessed: histological changes in the intestine, intestinal paracellular permeability (Ussing chamber), bursting pressure of the colonic anastomosis, and mitosis rate of the remnant liver. RESULTS: Bacterial translocation was observed in all rats, except in the sham group. Following liver resection, the highest bacterial concentrations were seen in liver and spleen, following colon anastomosis in the mesenteric lymph nodes. Bacterial translocation was increased in the animals with combined operation, in parallel to the extent of liver resection. In rats with colon anastomosis, bacterial concentration in the cecum was also higher than in the sham group. Application of probiotics significantly decreased bacterial concentration in the lymph nodes. In addition, animals with a high cecal concentration of lactobacilli had less translocation than the others. No histological changes were observed in the intestine. Paracellular permeability for ions, but not for the larger molecule lactulose, was increased in the colon in all groups with colon anastomosis. The bursting pressure of the colon anastomosis was not significantly different between the groups. Seventy percent liver resection led to a high rate of hepatocyte mitosis, whereas combination with colon anastomosis impaired the regeneration process. CONCLUSION: Synchronous liver resection and colon anastomosis led to increased bacterial translocation compared to the single operations in the rat model. It is possible to diminish this process by oral administration of probiotics. Bacterial overgrowth in the cecum and impaired hepatic regeneration, but not histological changes or alterations of paracellular permeability, are potential pathogenic mechanisms for translocation in this setting.

Administration, Oral↗
PubMed2002

Bacterial translocation in patients with Crohn's disease undergoing surgery.

PURPOSE: Much evidence, derived from experimental studies, suggests that bacterial translocation indeed occurs, yet its clinical significance is still a matter of controversy in humans. The aims of this study were to determine the prevalence of bacterial translocation in patients with Crohn's disease undergoing laparotomy and to identify any association with postoperative septic complications or systemic inflammatory response syndrome. METHODS: Mesenteric lymph node and peripheral blood samples from 42 patients with Crohn's disease undergoing laparotomy were collected for bacteriologic assessments. RESULTS: Bacterial translocation to mesenteric lymph node was identified in 20 patients (48 percent). The most common organism was (27 percent). Blood cultures were positive in 2 of 20 patients in whom translocation to lymph node was identified. Bacterial translocation was associated with a greater than two-fold increase in the incidence of postoperative septic complications (35 14 percent), but this difference was not significant. In the analysis of the occurrence of systemic inflammatory response syndrome, a significantly higher incidence continued until the third postoperative day in patients with those without bacterial translocation. In a logistic regression analysis, bacterial translocation had a significant effect on the occurrence of systemic inflammatory response syndrome, even though septic complications were taken into account. CONCLUSIONS: Bacterial translocation to mesenteric lymph node predisposed patients with Crohn's disease undergoing laparotomy to systemic inflammatory response syndrome.

Adolescent↗
PubMed1997

Bacterial translocation in multiple organ failure: cause or epiphenomenon still unproven.

BACKGROUND: A body of evidence exists for the occurrence of bacterial translocation and its relationship to multiple organ failure (MOF). METHODS: Relevant articles on bacterial translocation (the phenomenon defined as the passage of microbes and endotoxin across the intestinal barrier) in patients prone to develop MOF and in representative animal studies were selected. To interpret and evaluate the evidence for bacterial translocation in current literature, the endpoints generally used are discussed. RESULTS: Fractional data from individual manuscripts were tabulated and assessed for statistical significance with chi 2 analysis. Various clinically relevant stimuli, postulated as important causative factors for the development of MOF, appeared to be interrelated and related to bacterial translocation itself. CONCLUSIONS: Convincing evidence exists that bacterial translocation can occur in humans during various disease processes. However, it remains to be determined whether a causal relationship between bacterial translocation and MOF exists. MOF is probably multifactorial and not uniform in origin; when evaluating translocation as a causative factor in the absence of an infective focus, the type of initiating event and the period of time after which MOF develops should be taken into account. The origin of early MOF is probably a non-bacterial, extensive, inflammatory response resulting in massive generalized endothelial cell activation. Late MOF may be caused primarily by bacterial translocation inducing an imbalance between proinflammatory and anti-inflammatory cytokines.

Animals↗
PubMed2003

Bacterial translocation and its prevention in acute pancreatitis.

In recent years, bacterial translocation from the gut onto pancreatic necrosis has been proposed as the main cause of pancreatic infection and the consequent sepsis. Failure of the intestinal barrier, together with bacterial overgrowth due to motility changes and immunosuppression, constitute the pathways of the continuous pancreatic contamination from bacterial translocation in patients with severe acute pancreatitis. Selective decontamination, by using a combination of oral and intravenous antibiotics, has been reported to decrease the incidence of sepsis and the related mortality. Immunostimulation is another action to be taken to enhance the ability of the immune system to prevent bacterial translocation, by the entrapment and killing, by enterocytes, of the bacteria trying to translocate through the bowel wall. To keep the mucosal barrier function intact is one of the main issues in the prevention of bacterial translocation. This could be achieved by the adequate delivery of oxygen and nutrient supplementation. Enteral nutrition is a key factor, as it has been proven to maintain mucosal integrity, along with preventing deterioration of the immune function of the intestine.

Acute Disease↗
PubMed2004

Enteral administration of high-fat nutrition before and directly after hemorrhagic shock reduces endotoxemia and bacterial translocation.

OBJECTIVE: To determine whether potential enhancement of endotoxin neutralization via high-fat enteral nutrition affects endotoxemia and bacterial translocation after hemorrhage. SUMMARY BACKGROUND DATA: Endotoxin and bacterial translocation due to gut barrier failure are important initiating events in the pathogenesis of sepsis after hemorrhage. Systemic inhibition of endotoxin activity attenuates bacterial translocation and distant organ damage. Triacylglycerol-rich lipoproteins constitute a physiological means of binding and neutralizing endotoxin effectively. We hypothesized that enhancement of triacylglycerol-rich lipoproteins via high-fat enteral nutrition would reduce endotoxemia and prevent bacterial translocation. METHODS: A rat model of nonlethal hemorrhagic shock was used. Hemorrhagic shock (HS) rats were divided into 3 groups: rats starved overnight (HS-S); rats fed with a low-fat enteral diet (HS-LF), and rats receiving a high-fat enteral diet (HS-HF). RESULTS: Circulating triacylglycerol and apolipoprotein B, reflecting the amount of triacylglycerol-rich lipoproteins, were elevated in HS-HF rats compared with both HS-S rats (P <or= 0.005 and P <or= 0.05, respectively) and HS-LF rats (P <or= 0.005 and P <or= 0.05). Circulating endotoxin was lower in HS-HF rats (7.2 +/- 10.2 pg/ml) compared with both HS-S rats (29.1 +/- 13.4 pg/ml, P <or= 0.005) and HS-LF rats (29.9 +/- 5.2 pg/ml, P <or= 0.005). In line, bacterial translocation was lower in HS-HF rats (incidence 4/8 rats; median 3 [range 0-144] cfu/g) compared with both HS-S rats (8/8; 212 [60-483] cfu/g; P = 0.006), and HS-LF rats (8/8; 86 [30-209] cfu/g; P = 0.002). CONCLUSION: This study is the first to show that high-fat enteral nutrition, leading to increased plasma triacylglycerol and apolipoprotein B levels, significantly decreases endotoxemia and bacterial translocation after hemorrhage.

Animals↗
PubMed2002

Failure of Lactobacillus spp. to prevent bacterial translocation in a rat model of experimental cirrhosis.

BACKGROUND/AIMS: Prophylaxis of spontaneous bacterial peritonitis in cirrhotic patients with norfloxacin is associated with emergence of quinolone-resistant Enterobacteriaceae. We investigated whether an alternative strategy with Lactobacillus prevents bacterial translocation and ascitic fluid infection in cirrhotic rats. METHODS: CCl(4)-induced cirrhotic rats with ascites (n=34) were allocated to treatment with oral Lactobacillus strain GG at 1-2 x 10(9) cfu/day for 8-10 days (group LGG) or milk (group MILK). In addition, 20 cirrhotic rats were given a single dose of 15 mg norfloxacin orally and then allocated to Lactobacillus (group NOR-LGG) or milk (group NOR-MILK). Ten healthy rats served as control. After sacrifice the cecal flora were analyzed and the prevalence of bacterial translocation and ascitic fluid infection assessed. RESULTS: Cecal colonization with Lactobacillus was achieved in 90% of treated rats. The prevalence of bacterial translocation to mesenteric lymph nodes was 10% in control rats and 93, 84, 70 and 100% in groups MILK, LGG, NOR-MILK and NOR-LGG, respectively (P>0.1 for comparison of treatment groups), the prevalence of ascitic fluid infection was 60, 32, 40 and 40% (P>0.1). Bacterial translocation of Lactobacillus was observed in 24% of rats treated. CONCLUSION: Lactobacilli fail to prevent bacterial translocation and ascitic fluid infection in experimental cirrhosis in spite of successful intestinal colonization.

Animals↗
PubMed2005

Role of intestinal bacterial overgrowth and intestinal motility in bacterial translocation in experimental cirrhosis.

BACKGROUND: Intestinal bacterial overgrowth (IBO) is related to small bowel motility and has been involved in the pathogenesis of bacterial translocation (BT) in experimental models, and both overgrowing gut flora and translocating bacteria to mesenteric lymph nodes are common features in cirrhosis. OBJECTIVES: The aims of this study were to analyze cecal aerobic bacteria and intestinal transit in cirrhotic rats, and their relationship with BT, evaluating the role of intestinal bacterial overgrowth and small bowel dismotility in the development of BT in experimental cirrhosis. MATERIAL AND METHODS: We included twenty-seven male Sprague-Dawley rats with carbon tetrachloride-induced cirrhosis without ascites and ten controls. Cultures of mesenteric lymph nodes (MLN), peripheral and portal blood, liver, spleen and cecal samples were carried out. Small intestinal transit was determined in ten cirrhotic rats and in ten control rats. RESULTS: The prevalence of bacterial translocation was 56%. Total cecal aerobic bacteria count was significantly higher in cirrhotic rats than in control rats (p < 0.001). Cirrhotic rats with translocated bacteria had higher total aerobic intestinal counts than culture-negative MLN bacteria (p < 0.05). The prevalence of total intestinal bacterial overgrowth in cirrhotic animals was 67%, and 0% in control animals (p < 0.001). According to BT, total IBO was more frequent in cirrhotic rats with BT versus those without BT (93 vs. 33%) (p < 0.001). Of the translocating bacteria, 95.6% were found to be overgrown in the cecum. The small-intestinal transit was slower in cirrhotic rats (60.5 +/- 12.7 cm vs. 81.2 +/- 5.7 cm) than in control animals (p < 0.001). CONCLUSIONS: These results suggest that the increase of intestinal aerobic bacteria in experimental cirrhosis is associated with translocation. In addition, IBO is frequent in cirrhotic rats, and is supposed to play an important role in the development of BT. Impaired motility of the small intestine is a common feature in cirrhosis and may be implicated in the pathogenesis of IBO.

Analysis of Variance↗
PubMedDate not supplied

Effects of octreotide and a-tocopherol on bacterial translocation in experimental intestinal obstruction: a microbiological, light and electronmicroscopical study.

BACKGROUND/AIMS: Bacterial translocation induced by intestinal obstruction is suggested to be due to increased intestinal luminal volume, leading to intestinal overgrowth with certain enteric microorganisms and intestinal mucosal damage. If this suggestion is true, maintenance of intestinal mucosal integrity by a cytoprotective agent, a-tocopherol, and inhibition of gastrointestinal secretions by octreotide should decrease the incidence of bacterial translocation and extent of mucosal injury due to intestinal obstruction. METHODS: Complete intestinal obstruction was created in the distal ileum of male Wistar Albino rats by a single 3-0 silk suture. The animals received subcutaneous injections of 1 ml of physiologic saline (group 1) (PS 24) and 1 ml of saline containing octreotide acetate (100 micrograms/kg) (group 2) (OC 24), at 0, 12 and 24 hours of obstruction. In group 3 (PS 48) and group 4 (OC 48), the rats were treated with subcutaneous physiologic saline (1 ml) and octreotide acetate (100 micrograms/kg), respectively, beginning at the time of obstruction and every 12 hours for 48 hours. The rats in group 5 (Toc 24), were pretreated with intramuscular a-tocopherol 500 mg/kg on day 1 and 8, and underwent laparotomy on day 9. A third dose of a-tocopherol was injected at the time of obstruction on day 9 and no treatment was given thereafter. We tested the incidence of bacterial translocation in systemic organs and circulation and evaluated the histopathological changes in all groups. RESULTS: Treatment with octreotide acetate was found to be ineffective in reducing the incidence of translocation, with no histopathological improvement. Mucosal damage scores, on the other hand, in the a-tocopherol group were statistically less than those in the octreotide and control groups (p < 0.05). Additionally, a-tocopherol treatment decreased the incidence of organ invasion with translocating bacteria, although this difference did not reach statistical significance. CONCLUSION: Octreotide acetate treatment in complete intestinal obstruction has no effect on the incidence of bacterial translocation. a-Tocopherol, on the other hand, has a cytoprotective effect on intestinal mucosa in intestinal obstruction which, in turn, is thought to decrease bacterial translocation when used in physiological doses and prophylactically.

Animals↗
PubMed1993

Oral prostaglandin E2 prevents gut atrophy during intravenous feeding but not bacterial translocation.

The pathophysiologic changes in gut physiology that result in bacterial translocation during intravenous feeding are poorly defined, though believed to be related in part to intestinal atrophy, decreased mesenteric blood flow, and lack of intestinal secretions. This study investigated the hypothesis that pharmacologic preservation of intestinal structure and function by orally administered 16,16-dimethyl-prostaglandin E2 would prevent bacterial translocation in intravenously fed rats. Thirty-five rats were randomized to three groups: group 1 was fed rat chow ad libitum, group 2 received standard parenteral nutrition, and group 3 received parenteral nutrition plus oral 16,16-dimethyl-prostaglandin E2 (150 micrograms/kg twice a day). Rats were fed there respective diets for 5 days and killed. Mesenteric lymph nodes were procured for culture, and the intestine was assessed for weight, DNA, protein values, and histologic character. Results demonstrate that orally administered 16,16-dimethyl-prostaglandin E2 potently attenuates the intestinal atrophy associated with parenteral feeding but does not prevent bacterial translocation. Intestinal barrier dysfunction and bacterial translocation during intravenous feeding is related to factors other than the development of gut atrophy.

Administration, Oral↗
PubMed1997

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.

Animals↗