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PubMed2003

Rigid bronchoscopy induces bacterial translocation: an experimental study in rats.

Bronchoscopy has the potential to propagate infections. Bacterial translocation was hypothesised to be the cause of infections observed following bronchoscopy and this study was designed to assess the risk of bacterial translocation following rigid bronchoscopy in rats. A total of 30 rats were evaluated. The study group (n=15) underwent rigid bronchoscopy. Arterial blood gas analysis was performed in all rats. Blood and tissue cultures from the ileum, caecum, mesenteric lymph nodes, liver, spleen, mediastinal lymph nodes and lung were obtained 24 h following bronchoscopy. Bacterial translocation to the mesenteric lymph nodes was found in seven of 15 rats (46.7%) that underwent bronchoscopy, compared with none of the controls. Of the seven positives, three rats (42.8%) also demonstrated other organ involvement, such as the liver and spleen. Escherichia coli, Salmonella typhymirium, S. enteritidis and Pseudomonas spp. were found as translocating bacteria. In the study group, pH and arterial oxygen tension were significantly lower and arterial carbon dioxide tension was higher, compared with controls. This study shows that rigid bronchoscopy may induce bacterial translocation in rats. Further investigations aimed at understanding the clinical consequences of this phenomenon are warranted.

Animals↗

PubMed2006

T-cell inhibition does not aggravate bacterial translocation from rat small bowel.

BACKGROUND: T-cell mediated immunity has been proposed to have an important function in the defence against translocating microbes from the gastrointestinal tract. After small bowel transplantation massive T-cell immunosuppression is necessary to avoid rejection. As a consequence, infections with intestinal bacteria are the main contributors to mortality in this setting. This could further imply that T cells are important in limiting bacterial translocation. In a model for bacterial translocation from small bowel in the rat we examined the outcome of T-cell inactivation. METHODS: The studies were performed in a model of bacterial translocation from a Thiry-Vella loop of small bowel in the rat. The animals were treated with an anti-alpha/beta T-cell receptor monoclonal antibody (R73). Inhibition of T-cell activation was also made using the immunosuppressive drug cyclosporin A. All animals were sacrificed on day 3 postoperatively and translocation to the mesenteric lymph nodes, liver, spleen, lung and blood was evaluated. RESULTS: Treatment with R73 resulted in an almost complete labelling of T cells but did not result in any increased bacterial translocation compared to animals treated with saline. Neither did immunosuppression with cyclosporin A. CONCLUSIONS: In the model of bacterial translocation from a defunctionalised loop of small bowel the inhibition of T cells does not increase bacterial translocation to mesenteric lymph nodes or promote the systemic spread of the translocating bacteria. This indicates that T cells do not have any important protective function against translocating microbes from defunctionalised small bowel.

Animals↗

PubMed2003

Gastrointestinal disorders of the critically ill. Bacterial translocation in the gut.

The human gastrointestinal tract is colonized by a dense population of microorganisms, referred to as the bacterial flora. Although the gut provides a functional barrier between these organisms and the host, bacterial translocation is a common event in the healthy person. However, in critically ill patients, with various underlying diseases, this bacterial translocation may lead to infections and consequently to a further reduction in general health status. The mechanism of bacterial translocation is widely, and somehow controversially investigated in vitro and in animal models. In human studies, several diseases have been associated with bacterial translocation. However, methodological shortcomings, insufficient populations and conflicting results leave many open questions. This is also reflected in the various published therapeutic strategies. To overcome this problem more investigations in humans are needed, especially in techniques for detecting bacterial translocation.

Bacterial Translocation↗

PubMed1990

Food without fiber promotes bacterial translocation from the gut.

To determine whether the route and/or composition of nutritional support alters intestinal barrier function (measured as bacterial translocation), rats were divided into three groups: food (controls), intravenous total parenteral nutrition (IV-TPN) fed, and oral total parenteral nutrition (ORAL-TPN) fed. Bacterial translocation did not occur in the rats that were fed normally, but did occur in 60% of the rats fed the IV-TPN or the ORAL-TPN diets for 7 days (p less than 0.05). Since both the IV-TPN and ORAL-TPN diets induced bacterial translocation and the TPN solution (28% glucose and 4.5% amino acids) lacks fiber, two additional groups of rats were fed orally 2.5 gm cellulose powder/day plus TPN solution by either the intravenous or the oral route. The addition of cellulose powder decreased the incidence of bacterial translocation to 8% in the group fed the ORAL-TPN diet and to 0% in the group fed the IV-TPN diet. Cellulose improved intestinal barrier function, even though it did not prevent bacterial overgrowth or the loss of mucosal mass in the rats fed the IV-TPN or ORAL-TPN diets. Cellulose powder appears to have prevented bacterial translocation primarily by preventing IV-TPN- or ORAL-TPN-induced alterations in mucosal structure. Thus the oral administration of this fiber maintains intestinal barrier function and prevents bacterial translocation even in the absence of oral nutrients.

Administration, Oral↗

PubMedDate not supplied

Gut decontamination prevents bronchoscopy-induced bacterial translocation. An experimental study in rats.

BACKGROUND: Selective gut decontamination is suggested to suppress the gram-negative bacterial overgrowth in the intestine and consequently to reduce bacterial translocation. OBJECTIVE: The purpose of the present study is to examine the effects of gut decontamination on bronchoscopy-induced bacterial translocation, and intestinal mucosal injury. METHODS: Forty-five rats were assigned into three groups. Group 1 served as control (n=15). Group 2 (n=15) and group 3 (n=15) underwent bronchoscopy. In addition, group 3 underwent gut decontamination. Gut decontamination was performed two days prior to bronchoscopy with erythromycin and neomycin. Twenty-four hours after bronchoscopy, blood, mesenteric lymph nodes, spleen, liver, ileum and cecum were harvested for bacterial determination. The ileum was also assessed and graded histologically according to Chiu's injury scale. RESULTS: In the bronchoscopy group, bacterial translocation to the mesenteric lymph nodes was found in 7/15 rats (46.7%), compared to none of the controls (p=0.01). These rats also showed significant evidence of intestinal injury, compared to the controls (mean ranks, 32.7 or 8.5, p<0.0001). On the other hand, gut decontamination prevented bacterial translocation, compared to the bronchoscopy group (p=0.011). However, gut decontamination provided no beneficial effect on the intestinal mucosal injury, compared to the bronchoscopy group. These animals also revealed significant intestinal injury, compared to the controls (mean ranks, 27.8 or 8.5, p<0.0001). CONCLUSIONS: Our data shows that despite no amelioration in bronchoscopy-induced intestinal mucosal injury, gut decontamination has a preventive role for bronchoscopy-induced bacterial translocation.

Animals↗

PubMed1997

Effect of Lactobacillus supplementation with and without arginine on liver damage and bacterial translocation in an acute liver injury model in the rat.

In acute liver failure following hepatitis, toxic insults, or after major liver surgery, there is an increased bacterial translocation from the gut. This may explain some of the infectious complications seen in these conditions. To elucidate mechanisms and find possible preventive measures, we investigated the effect of rectal administration of arginine and probiotic bacteria (Lactobacillus spp.) on bacterial translocation and the extent of liver failure. Sprague-Dawley rats were used and five different Lactobacillus strains (Lb. reuteri R2LC, Lb. rhamnosus DSM 6594 (= strain 271), Lb. plantarum DSM 9843 (= strain 299v), Lb. fermentum 8704:3 (= strain 245), and Lb. reuteri (= strain 108) were administered rectally once daily for 8 days with and without 2% arginine. Acute liver injury (ALI) was induced on the eighth day by intraperitoneal injection of D-galactosamine (1.1 g/kg body weight), and samples were collected after 24 and 48 hours. Bacterial translocation was evaluated by bacterial culture from portal and arterial blood, mesenteric lymph nodes, and liver tissue. Liver enzymes and bilirubin were evaluated in the serum. The bacterial load in the cecum and colon was determined and the liver histopathological changes were studied. There was no mortality at any time. The liver enzymes and bilirubin decreased in some of the groups supplemented with lactobacilli with and without arginine compared with the ALI control group. The incidence of bacterial translocation and the number of the translocated bacteria decreased significantly in some of the supplemented groups. Lb. plantarum + arginine administration significantly reduced the level of the released liver enzymes, hepatocellular necrosis and inflammatory cell infiltration, bacterial translocation, and the number of Enterobacteriaceae in the cecum and colon. Rectal administration of different Lactobacillus strains with and without arginine in an ALI model significantly modulates the extent of the liver failure and reduces bacterial translocation. Lb. plantarum DSM 9843 (= strain 299v) with or without arginine seemed superior to the other Lactobacillus strains. The beneficial effect of arginine administration alone indicates a possible role of nitric oxide and polyamines in this process, and the lactobacilli may execute their action via the same mechanisms or via bacterial antagonism and/or enhancement of systemic and intestinal mucosal immunity.

Alanine Transaminase↗

PubMed2005

The effects of ketamine and propofol on bacterial translocation in rats after burn injury.

BACKGROUND: Bacterial translocation (BT) occurs after thermal injury and may result from an ischemic intestinal insult. The aim of the study was to investigate the effects of ketamine and propofol as anesthetic agents on BT in an animal model of burn injury. METHODS: Sixty male Wistar Albino rats were randomly assigned to six groups of 10 rats each. Anesthesia was induced and maintained with ketamine in groups 1, 2 and 3 and with propofol in groups 4, 5 and 6 during 6 h. Groups 2, 3, 5 and 6 received 30% total body surface area (TBSA) third-degree burns. Groups 1 and 4 had no burn injury. Then, they were allowed to recover from the anesthesia at the end of 6 h. Mean arterial pressure (MAP) was monitored continuously and maintained within 10% of baseline (before burn injury) levels in all animals. Animals in groups 3 and 6 had a laparotomy to obtain a tissue sample from the terminal ileum for determination of intestinal lipid peroxidation by-product malondialdehyde (MDA) before (baseline) and 6 and 24 h after burn injury (ABI). So these animals were not included in the BT studies. At postburn 24 h, animals in groups 1, 2 and 4, 5 were sacrified and samples were taken from the mesenteric lymph nodes (MLN), liver and spleen for bacteriologic cultures. RESULTS: The incidence of BT was found to be significantly higher in group 2 than in all the other groups. Bacterial translocation incidence of group 5 was not significantly different from that of groups 4 and 1. Group 5 was associated with a significantly reduced number of enteric organisms per gram of tissue compared to group 2. Baseline MDA contents of groups 3 and 6 were similar. Ileal MDA levels were increased in group 3, but there were no significant changes in group 6 at 6 and 24 h ABI compared to baseline. CONCLUSION: Our results suggest that propofol as an anesthetic agent may prevent BT by scavenging reactive oxygen species and inhibiting lipid peroxidation in an animal model of burn injury.

Analgesics↗

PubMed1996

The effect of minimum luminal nutrition on bacterial translocation and atrophy of the jejunum during parenteral nutrition.

In situations of catabolic stress, the gut becomes atrophic and may have diminished barrier function as evidenced by an increase in bacterial translocation. The aim of this study was to examine the effect of minimum luminal nutrition during parenteral nutrition on the extent of jejunal atrophy and rate of bacterial translocation. Central venous lines were inserted into 30 rats before they underwent randomization to receive nutritional support with: (a) conventional parenteral nutrition; (b) conventional parenteral nutrition with 3 g/day of rat food (i.e., minimum luminal nutrition); or (c) rat food ad libitum. The rats were assessed after 10 days for nutritional status, extent of jejunal atrophy, caecal flora, as well as the extent of bacterial translocation to the mesenteric lymph nodes, liver and spleen. Rats in the rat food ad libitum group lost the smallest amount of weight and had the least amount of jejunal atrophy, yet had a similar rate of bacterial translocation as the parenterally nourished groups. When compared with the conventional parenteral nutrition group, the minimum luminal nutrition group had better preservation of the weight of the small bowel and its isolated mucosa (P < 0.01), but had a similar rate of bacterial translocation. Minimum luminal nutrition reduced the extent of atrophy of the gut but did not affect the incidence of bacterial translocation. It is inferred that there is no direct relationship between the extent of mucosal atrophy and incidence of bacterial translocation.

Animal Feed↗

PubMed1990

Effect of hemorrhagic shock on bacterial translocation, intestinal morphology, and intestinal permeability in conventional and antibiotic-decontaminated rats.

Bacterial translocation and ileal and cecal injury have been shown to occur 24 h after limited periods of hemorrhagic shock. The present studies were performed to determine the temporal sequence of mucosal injury, permeability, and bacterial translocation after hemorrhagic shock. The results indicated that bacterial translocation and mucosal injury have occurred by 2 h after a 30-min episode of shock (mean arterial pressure 30 mm Hg). Although the histologic extent of the intestinal mucosal injury was less at 2 h postshock than at 24 h postshock, at both times intestinal barrier function was lost as measured by permeability to horseradish peroxidase. Since the role of translocating bacteria in potentiating the loss of intestinal barrier function after shock is unclear, the second goal was to determine whether the extent of shock-induced mucosal injury and permeability could be reduced or abrogated by antibiotic decontamination of the gut. The extent of shock-induced mucosal injury and intestinal permeability was similar between rats with a normal gut flora (greater than 10(6) bacteria/g cecum) and antibiotic-decontaminated rats (less than 10(3) bacteria/g cecum) 2 h postshock, although the incidences of bacterial translocation were 67% and 0, respectively. Thus, shock-induced mucosal permeability and injury appear not to be directly related to the presence of translocating bacteria.

Animals↗

PubMed2000

Bacterial translocation and tumor necrosis factor-alpha gene expression in experimental hemorrhagic shock.

OBJECTIVE: To investigate whether bacterial translocation is the causative mechanism underlying cytokine production during hemorrhagic shock. DESIGN: Prospective, randomized, unblinded animal study. SETTING: Surgical research laboratories of Shiga University of Medical Science. SUBJECTS: Male Sprague-Dawley rats. INTERVENTIONS: The rats were randomly divided into three groups. Each animal was anesthetized with pentobarbital, given a continuous infusion of 0.9% saline, and monitored for blood pressure. The normoxic and sham shock groups breathed room air, whereas the hyperoxic shock group was administered 100% oxygen. Except in the sham shock group, blood was withdrawn to induce a hemorrhagic shock state, then the shed blood was reinfused. Sixty minutes after the induction of hemorrhagic shock, arterial blood cultures were performed in all three groups. The animals were then killed, and their mesenteric lymph nodes (MLNs) were harvested for bacterial culture. The terminal ileum, liver, spleen, kidney, lung, and MLNs were also collected for histologic study by in situ hybridization. MEASUREMENTS AND MAIN RESULTS: In the bacteriologic study, the prevalence of bacterial translocation was 0% (0/11) in the hyperoxic shock group, 55% (6/11) in the normoxic shock group, and 0% (0/9) in the sham shock group. In the in situ hybridization study, tumor necrosis factor-alpha gene expression was detected only in the ileal tissue, MLNs, and spleens of the normoxic shock group. Blood cultures were sterile in all three groups. CONCLUSIONS: Bacterial translocation occurred in MLNs within 1 hr of hemorrhage. Hemorrhagic shock causes tumor necrosis factor-alpha gene expression as well as bacterial translocation in MLNs, but not in the liver, in this model. Bacterial translocation was prevented by hyperoxia early in the course of hemorrhagic shock. Hyperoxia also prevented tumor necrosis factor-alpha gene expression along the bacterial invasion route.

Animals↗

PubMed1993

Bacterial translocation and reticuloendothelial function after implantation of abdominal drainage in the rat.

Bacterial translocation and reticuloendothelial system (RES) function were measured in the rat after intraperitoneal (IP) implantation of rubber drain pieces (7.5 cm2). Six hours after implantation, enteric bacterial translocation was noted to mesenteric lymph nodes (MLNs), the liver, spleen, lungs, kidneys and portal and caval vein blood. RES function was evaluated in terms of blood clearance and organ uptake of intravenously injected 125I-labelled, heat-killed E. coli. A significant elevation of corrected phagocytic index (alpha) was found 24 hours after IP implantation. Localization of 125I-labeled E. coli was significantly enhanced in systemic organs (kidneys, spleen, liver and lungs) 24 hours after IP implantation, whereas it was locally impaired (MLNs and proximal jejunum) 6 hours after IP implantation and thereafter. An inverse correlation between the localization of radiolabelled E. coli in the liver, spleen and lungs and the incidence of bacterial translocation to these organs was found. The results suggest that an association exists between alterations in RES function and bacterial translocation in the early course following IP implantation of rubber drains.

Abdomen↗

PubMed1993

Elemental diet-induced bacterial translocation and immunosuppression is not reversed by glutamine.

Previously, we documented that bacterial translocation occurs in rats fed an elemental liquid diet (4.25% amino acids plus 28% glucose) for 7 days. Since controversy exists over the protective effect of glutamine on diet-induced bacterial translocation, we compared the effect of two elemental diets, one containing 0% and the other 30% of amino acids as glutamine. After 7 days on the test diets or chow (307 kcal/kg/day), the rats were killed and half the animals had their organs cultured for translocating bacteria; immune function was quantitated in the other half by measuring the blood, splenic, and mesenteric lymph node (MLN) blastogenic responses to the T-cell mitogens phytohemagglutinin (PHA) and concanavalin A (ConA). The incidence of bacterial translocation was higher in the rats fed the glutamine (88%) or nonglutamine (75%) elemental diets than in the chow-fed rats (13%) (p < 0.05). Both elemental diets equally reduced the blastogenic response of lymphocytes harvested from all three lymphoid compartments (blood, spleen, MLN) (p < 0.01 vs. chow). The percentage of reduction averaged 30% to 40% when PHA was used as the test mitogen and 50% to 70% when ConA was used. These results indicate that glutamine does not prevent elemental diet-induced bacterial translocation or immune suppression.

Animals↗

PubMedDate not supplied

The effects of sodium deoxycholate, lactulose and glutamine on bacterial translocation in common bile duct ligated rats.

BACKGROUND/AIMS: Sepsis is a major cause of post-operative morbidity and mortality in obstructive jaundice as a result of bacterial translocation from the gut. This study was conducted to investigate the effects of glutamine, lactulose, and the bile salt Na deoxycholate in preventing bacterial translocation in an animal model where obstructive jaundice was developed by common bile duct ligation. METHODOLOGY: Fifty Wistar albino rats were divided into 5 groups of 10 animals each. The animals in groups I-IV underwent common bile duct ligation and received, respectively, either saline, Na deoxycholate, lactulose or glutamine, orally. Group V had sham ligation and received saline orally. The animals were sacrificed at the end of the 7th day, and serum concentrations of bilirubin, aspartate aminotransferase (ALT), alanine aminotransferase (ALT), and alkaline phosphatase (AP) were measured. In addition, mesenteric lymph nodes were removed and cultured together with cecal content. Histopathologic examination of terminal ileum specimens was made. RESULTS: Na deoxycholate, lactulose and glutamine all reduced bacterial translocation rates to mesenteric lymph nodes (p<0.05), with glutamine causing the greatest effect. Na deoxycholate and lactulose prevented bacterial translocation by causing a decrease in cecal intraluminal bacterial content (p<0.001), while glutamine exerted its effect by preserving intestinal mucosal integrity. CONCLUSIONS: The integrity of the intestinal mucosal barrier is of paramount importance in preventing bacterial translocation, and the measures taken to protect mucosal integrity reduce bacterial translocation to a greater extent than those taken to decrease the number of bacteria in the gut.

Animals↗

PubMed2005

[Bacterial translocation and its clinical significance].

Bacterial translocation (BT) is defined as the passage of indigenous bacteria colonizing the intestine through the epithelial mucosa to the mesenteric lymph nodes and other sites. It can even cause the development of lethal sepsis. BT is being studied extensively, most research being conducted on animal, mostly murine, models. The cause of BT is not well known. Despite advances in antimicrobial therapy, the mortality rate associated with bacteremia is still high, and sepsis can often originate from the patient's own intestinal flora. Consequently, a better understanding of the mechanisms of BT as well as mechanisms operating to prevent bacteria from translocating from the gastrointestinal tract may provide more logical treatment of particular patients. BT may be promoted by immunosuppression (probably one of the most important factors causing the increase in BT), disturbances in the normal ecology of the gastrointestinal tract, allowing some indigenous bacteria to overgrow others, and by mucosal injuries. This article discusses the potential role of various factors responsible for BT and the relationship between BT and neoplastic disease. It also emphasizes the significance of the immune system, which appears to play a role in the ontogeny of gut-associated lymphoid tissue (GALT), including the role of IL-2 (which induces an increase in BT) and the macrophage, which participates in the transport of bacteria from the intestinal lumen to mesenteric lymph nodes. A better understanding of the immunopathology of BT may contribute to the development of novel means of therapy for sepsis and other serious complications of bacterial infection.

Animals↗

PubMed1992

The degree of bacterial translocation is a determinant factor for mortality after burn injury and is improved by prostaglandin analogs.

Bacterial translocation and related mortality rates were examined in previously transfused BALB/c mice that were gavaged with 14C radioisotope-labeled Escherichia coli before inflicting a 20% full-thickness flame burn. Radionuclide counts were measured in blood obtained by retro-orbital puncture 4 hours postburn, and survival was recorded for 10 days. Radionuclide counts in the blood correlated well with both radionuclide counts and numbers of viable bacterial in the tissues. Survivors had significantly less bacterial translocation as evidenced by blood radionuclide counts compared with nonsurvivors, and there was a significant inverse correlation between the degree of translocation and the length of survival. In the next experiment, the prostaglandin E (PGE) analogs misoprostol, enisoprost, or 16,16-dimethyl PGE2 were administered to transfused animals for 3 days before burn. Prostaglandin E analogs significantly reduced bacterial translocation as measured by blood radionuclide counts 4 hours postburn and improved survival. The data demonstrate that the intensity of bacterial translocation after burn injury is significantly associated with subsequent death. Improvement of survival by PGE analogs is associated with decreased bacterial translocation.

16,16-Dimethylprostaglandin E2↗

PubMedDate not supplied

[Bacterial translocation: the effect of supplements with dietary fiber in enteral diets in an experimental model of methotrexate-induced enterocolitis].

Bacterial translocation, described by 1979 by Berg and Garlington as the movement of viable bacteria through anatomically intact intestinal mucosa to the mesenteric ganglia, is suspected of playing an important role in the development of sepsis with no apparent focus, fundamentally in polytraumatized and sever surgical patients: even now, with the wide range of antibiotic and chemotherapy agents available for treatment, this sepsis represents a high rate of hospital morbid-mortality. To assess the function as barrier of the intestinal mucosa and the influence of dietary fiber thereon, we studied bacterial translocation measured as positive cultures of the mesenteric lymphatic ganglia in an experiment model of enterocolitis induced by the intraperitoneal injection of 20 mg/kg of Methotrexate (MTX), using 72 male S-D rats, half of which were used as control group. These animals were sub-divided into four series according to the diet they were to receive. In addition to bacterial translocation, we examined the intestinal mucous parameters (mucosa weight, protein and DNA content, and number of mitoses) to quantify the potential trophic effect of dietary fiber on the intestinal mucosa. In the group subject to enterocolitis, there were no significant differences in the bacterial translocation with the series fed with defined-formula diets supplemented or otherwise with dietary fiber. Only the series receiving standard feed showed a significant reduction of bacterial translocation. pectin improved all mucous parameters when compared with the other diets studied. In the control group, the bacterial translocation rate was zero in all dietary series.

Analysis of Variance↗

PubMed2004

[Strategy for bacterial translocation in acute pancreatitis].

Although bacterial translocation (BT) is thought to be a main cause of secondary pancreatic infection, the clinical significance is still unclear. Therefore, we investigated relationship between pancreatic infection and BT, analyzing the results of treatments such as continuous regional arterial infusion of protease inhibitor and antibiotics (CRAI), selective digestive decontamination, and early enteral nutrition (SDD/EN) in 45 severe acute pancreatitis patients. The infection rate of 17 cases without CRAI, SDD/EN was 58.8%, and mortality was 23.5%. Antibiotics-resistant bacteria, such as methicillin-resistant Staphylococcus aureus (MRSA) was often proven in infected pancreatic tissue. Whereas, in 16 cases who underwent both therapy, only one patient died of multi-organ failure (6.3%). Pseudomonas aeruginosa and K. pneumoniae were proven from his feces before pancreatic infection coincidence, and, in autopsy, these bacteria and MRSA were proved from necrotic pancreatic tissue. BT must be large cause of secondary pancreas infection, because CRAI and SDD/ EN prevent secondary pancreatic infection. But we must consider other infection routes, and development of antibiotics resistant bacteria.

Acute Disease↗

PubMed1994

Secretory immunoglobulin A, intestinal mucin, and mucosal permeability in nutritionally induced bacterial translocation in rats.

OBJECTIVE: The authors investigated the role of mucin and secretory immunoglobulin A (slgA) in a model of nutritionally induced bacterial translocation. BACKGROUND: Parenteral and certain elemental diets have been shown to impair intestinal barrier function, whereas fiber has been shown to protect against nutritionally induced bacterial translocation. However, the factors responsible for these phenomenon have not been fully determined. METHODS: Intestinal mucin levels, mucosal protein content, slgA, intestinal morphology, and permeability to horseradish peroxidase, bacterial translocation, and intestinal bacterial population levels were measured in rats 7 days after receiving total parenteral nutrition (TPN) solution (28% glucose, 4.25% amino acids; 307 kcal/kg/day) enterally (ORAL-TPN) or parenterally (IV-TPN) with or without enteral bulk fiber supplementation. Chow-fed rats served as control subjects. RESULTS: The incidence of bacterial translocation in the ORAL-TPN and IV-TPN groups was reduced significantly by the provision of fiber (p < 0.05). Mucosal protein, slgA, and insoluble mucin levels were decreased in the jejunum of the ORAL-TPN and IV-TPN groups, with mucosal protein levels being decreased to a greater extent than slgA or mucin. Although similar decreases in these parameters were observed in the fiber-fed groups, fiber appeared to improve intestinal barrier function as measured by horseradish peroxidase permeability. CONCLUSIONS: The provision of bulk-forming fiber improves intestinal barrier function as measured by peroxidase permeability and bacterial translocation, but does not restore mucosal protein content, intestinal mucin, or slgA levels to normal.

Animals↗