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Edwin A Deitch - One of the best experts on this subject based on the ideXlab platform.
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elemental diet induced Bacterial Translocation associated with systemic and intestinal immune suppression
Journal of Parenteral and Enteral Nutrition, 1998Co-Authors: Edwin A DeitchAbstract: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 IV 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 IV 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 subgroup 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.
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elemental diet and iv tpn induced Bacterial Translocation is associated with loss of intestinal mucosal barrier function against bacteria
Annals of Surgery, 1995Co-Authors: Edwin A Deitch, Markus B Naruhn, David C Deitch, Andrew A MarinoAbstract:OBJECTIVE: The goal of the current study was to directly assess the role of loss of mucosal barrier function in nutritionally induced Bacterial Translocation. BACKGROUND: Parenteral and certain elemental enteral diets have been shown to promote Bacterial Translocation. The mechanisms underlying this observation, especially the question of whether nutritionally induced Bacterial Translocation is primarily related to loss of intestinal barrier function, versus an impaired immune system, remain to be fully elucidated. METHODS: Bacterial Translocation was measured in vivo, ileal mucosal membranes were harvested, and their electrophysiologic properties and barrier function were measured ex vivo in the Ussing chamber system 7 days after receiving total parenteral nutrition solution parenterally (IV-TPN) or enterally (elemental diet). Chow-fed rats served as control subjects. RESULTS: The incidence of Bacterial Translocation was significantly increased both to the mesenteric lymph nodes in vivo and across the in vitro Ussing chamber-mounted ileal mucosal membranes of the elemental diet-fed and IV-TPN-fed rats. The magnitude of Escherichia coli and phenol red transmucosal passage in the Ussing chamber was significantly higher in the IV-TPN-fed rats than in the elemental diet-fed or chow-fed animals. The potential differences across the ileal membrane were similar between the three groups at all time points. However, the specific resistances of the ileal membranes of the IV-TPN and elemental diet groups were significantly less than the chow-fed animals, indicating increased membrane permeability. CONCLUSIONS: Loss of intestinal barrier function plays a major role in nutritionally induced Bacterial Translocation, and the loss of mucosal barrier function to both E. coli and phenol red appeared greater in the IV-TPN than the elemental diet-fed rats.
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the modulatory role of gut hormones in elemental diet and intravenous total parenteral nutrition induced Bacterial Translocation in rats
Journal of Parenteral and Enteral Nutrition, 1994Co-Authors: Yuval Haskel, Edwin A DeitchAbstract:We have previously shown that parenteral and certain elemental diets promote Bacterial Translocation and that this diet-induced Bacterial Translocation can be prevented by the provision of bulk-forming dietary fiber. The goal of the current study was to test the hypothesis that fiber's protective effect on diet-induced Bacterial Translocation was mediated by trophic gut hormones. This hypothesis was tested by using bombesin (which stimulates gut hormone release) or the somatostatin analog Sandostatin (which inhibits gut hormone release) to modulate gut hormone release in rats receiving rat food, intravenous total parenteral nutrition, or an elemental diet. Both bombesin and fiber were effective in preventing elemental diet-induced Bacterial Translocation, whereas octreotide acetate abrogated the protective effect of fiber. Bombesin was also effective in limiting Bacterial Translocation in parenterally fed rats. Although both enteral (elemental diet) and parenteral diet-induced Bacterial Translocation were...
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elemental diet induced Bacterial Translocation can be hormonally modulated
Annals of Surgery, 1993Co-Authors: Yuval Haskel, Edwin A DeitchAbstract:BACKGROUND: The authors have previously documented that feeding mice an elemental diet resulted in Bacterial Translocation (BT) that could be prevented by the provision of dietary fiber. To test whether the protective effect of fiber was related to the stimulation of trophic gut hormones, the effects of sandostatin and bombesin were tested. METHODS: Mice fed either chow or the elemental diet were stratified into several groups and the ability of bombesin (10 micrograms/kg, tid) or sandostatin (100 micrograms/kg bid) to modulate BT was examined. After 14 days, mice were sacrificed and BT, cecal Bacterial population levels, mucosal protein, and small bowel weight was measured. Segments of the ileum and jejunum were examined histologically. RESULTS: Incidence of elemental diet-induced BT (75%) was reduced by fiber (9%) or the administration of bombesin (13%) (p < 0.01). Although sandostatin did not promote BT in chow-fed mice, it reversed the protective effect of fiber on BT (75%) (p < 0.01). CONCLUSION: Elemental diet-induced Bacterial Translocation can be modulated hormonally and the beneficial effects of fiber on diet-induced BT appears to be hormonally mediated.
Stig Bengmark - One of the best experts on this subject based on the ideXlab platform.
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Bacterial Translocation intestinal ultrastructure and cell membrane permeability early after major liver resection in the rat
British Journal of Surgery, 2005Co-Authors: Xiangdong Wang, Roland Andersson, H Parsson, Vasile Soltesz, Kjell Johansson, Stig BengmarkAbstract:The process and route of Bacterial Translocation from the gut after major liver resection remain unclear. In the present study enteric Bacterial Translocation, enterocyte ultrastructure in the ileum and colon, the process and route of Bacterial invasion and the permeability of the cell membrane system and blood-tissue barrier were evaluated in rats receiving sham operation, and 70 or 90 per cent hepatectomy. The incidence of Bacterial Translocation to mesenteric lymph nodes was 80-100 per cent in rats 6 h after 70 per cent and 2-4 h after 90 per cent hepatectomy, and 80-100 per cent to the systemic circulation 2-4 h after 90 per cent hepatectomy but only 20 per cent to the portal vein. An increase in Bacterial adherence to the intestinal surface, damage to the permeability of the cell membrane system and blood-tissue barrier, and pathological alterations in the ileum and colon developed, correlating with the extent of liver removed and the time that had passed after hepatectomy. Most translocating bacteria appeared in morphologically intact enterocytes with increased membrane permeability, in antigen-presenting cells and in submucosal lymphatics, but some bacteria were also seen within damaged enterocytes 4h after 90 per cent hepatectomy. These results indicate that altered permeability of the cell membrane system may be one of the earliest characteristics of challenged enterocytes, and that enteric bacteria translocate through both morphologically normal and abnormal enterocytes. Translocation occurred mainly into the lymphatics, bacteria either being 'carried' by antigen-presenting cells or entering by active invasion.
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orally administered phospholipids inhibit abdominal rubber drain induced Bacterial Translocation in the rat
Digestion, 1994Co-Authors: Roland Andersson, Åsa Ljungh, H Parsson, Kjell Johansson, Stig BengmarkAbstract:In order to determine the influence of phospholipid on abdominal biomaterial-induced Bacterial Translocation (BT), phsophatidylcholine (PC) or phos-phatidylinositol (PI) was administered orally or intraperitoneally in rats with intraperitoneal implantation of 7-cm2 rubber drain pieces. Two days after surgery, the incidence of Translocation to mesenteric lymph nodes and liver significantly decreased, the adherence of 3H-labeled Escherichia coli to the ileal mucosa was signifciantly inhibited and the phagocytic and bactericidal capacity of peritoneal macrophages increased in animals with PC or PI administered orally, but not intraperitoneally, as compared with rats without phospholipid administration. Scanning electron microscopy revealed a coating layer on the surface of the intestinal mucosa in phospholipid-gavaged rats. Thus, the results in the present study imply that oral, but not intraperitoneal, PC of PI administration reduces enteric BT induced by intraperitoneal drain implantation.
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phospholipid impregnation of abdominal rubber drains resistance to Bacterial adherence but no effect on drain induced Bacterial Translocation
Research in Experimental Medicine, 1993Co-Authors: Roland Andersson, Åsa Ljungh, Rolf Odselius, Torkel Wadstrom, Stig BengmarkAbstract:In order to evaluate the effect of surface modification of biomaterials on Bacterial adherence and Bacterial Translocation after intraperitoneal biomaterial implantation, phosphatidylcholine- or phosphatidylinositol-impregnated rubber drain pieces, which had been intraperitoneally implanted in the rat for 2 and 7 days, or unimplanted, were incubated in vitro with3H-labelledEscherichia coli andEnterobacter cloacae. As compared with unimpregnated pieces, the adherence of bacteria significantly decreased to phosphatidylcholine- and phosphatidylinositol-impregnated rubber drain pieces that were either unimplanted or implanted for 2 days, but not for 7 days. The supplementation of albumin in the medium reduced the adherence of bacteria to the unimplanted, unimpregnated drain pieces, but did not further decrease adherence of bacteria to the unimplanted, phospholipid-impregnated brain pieces. Bacterial growth was inhibited after incubation in nutrient broth supplemented with phospholipids. The incidence of enteric Bacterial Translocation induced by intraperitoneal drain implantation did not differ between phospholipid-impregnated and unimpregnated drain pieces. Scanning electron microscopy revealed a large amount of biofilm and fibrous deposition on the surface of the implanted, phospholipid-impregnated rubber drain pieces. Thus, phospholipid impregnation of rubber drains reduces Bacterial adherence and inhibits Bacterial growth, without influencing the incidence of Bacterial Translocation.
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Bacterial Translocation into portal blood from the gut during portal triad occlusion
Digestive Surgery, 1992Co-Authors: Bengt Jeppsson, Stig BengmarkAbstract:Bacterial Translocation into portal blood from the gut could be detected as early as 15 min following portal triad occlusion (PTO) in rats and increased with the increasing length of PTO. The peak of
Guadalupe Garciatsao - One of the best experts on this subject based on the ideXlab platform.
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Bacterial Translocation bt in cirrhosis
Hepatology, 2005Co-Authors: Reiner Wiest, Guadalupe GarciatsaoAbstract:Gut flora and Bacterial Translocation (BT) play an important role in the pathogenesis of the complications of cirrhosis. Research on the pathogenesis of BT and its clinical significance transcends established boundaries between microbiology, cell biology, intestinal pathophysiology, and immunology. This review delineates multiple mechanisms involved in the process of BT, with an emphasis on alterations in intestinal flora and mucosal barrier function, particularly immunological defense mechanisms. Current knowledge on the innate and adaptive immune response that allows a "friendly" communication between bacteria and host is summarized, and alterations occurring in cirrhosis that may facilitate BT are discussed. In addition, definition of a "pathological" BT is proposed together with an analysis of the anatomical site and route of BT. Finally, therapeutic approaches for the prevention of BT in experimental and human cirrhosis are reviewed. Future research in the field of BT in cirrhosis will allow the development of new therapeutic targets in the prevention of infections and other complications of cirrhosis.
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effect of lactobacillus fermented diets on Bacterial Translocation and intestinal flora in experimental prehepatic portal hypertension
Digestive Diseases and Sciences, 2003Co-Authors: Reiner Wiest, Guadalupe Garciatsao, F Chen, Gregory W Cadelina, Roberto J GroszmannAbstract:Spontaneous Bacterial infections in cirrhosis and portal hypertension have been attributed to trans- location of gut-derived bacteria, a process promoted by intestinal Bacterial overgrowth and disruption of the gut mucosal barrier. Bacteriotherapy with Lactobacillus has been reported to correct Bacterial overgrowth, stabilize mucosal barrier function, and decrease Bacterial Translocation in rat models of acute liver injury and failure. In this study we investigated the effect of Lactobacillus-supplemented diets on intestinal flora and on Bacterial Translocation rate in portal vein ligated rats. Lactobacillus-fermented milk (yogurt) containing at least 2 × 109 colony forming units/ml or placebo (water) was adminstrated by gavage twice daily (2 ml) for 9 days. Portal vein ligation was performed on day 7 of treatment. Bacterial Translocation to mesenteric lymph nodes and quantification of intestinal flora was assessed by standard bacteriological cultures. Bacterial Translocation was not significantly different between animals that received yogurt (82%) and those that received placebo (75%). Yogurt did not induce any significant changes in intestinal flora, whether it was produced with Lactobacillus acidophilus or Lactobacillus GG. In conclusion, in acute prehepatic portal hypertension, bacteriotherapy with Lactobacillus was unable to induce changes in Bacterial Translocation probably because it was unable to induce changes in Bacterial flora.
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Bacterial Translocation to mesenteric lymph nodes is increased in cirrhotic rats with ascites
Gastroenterology, 1995Co-Authors: Guadalupe Garciatsao, Fayauh Lee, G E Barden, Richard W Cartun, A B WestAbstract:Abstract Background/Aims: Cirrhotic patients are predisposed to develop spontaneous bacteremias and/or peritonitis, mainly caused by enteric bacteria. The aim of this study was to investigate if Bacterial Translocation, which is the passage of bacteria from the intestinal lumen to regional lymph nodes and/or the systemic circulation, is increased in a rat model of cirrhosis. Methods: Rats were studied after 12–16 weeks of CCl 4 inhalation, when samples of mesenteric lymph nodes, blood, liver, and spleen for standard bacteriologic cultures and a fragment of colon and liver for histology were obtained. Immunostaining of the cecum was performed using a polyclonal anti- Escherichia coli antibody. Results: A significantly greater proportion of rats with cirrhosis and ascites (5 of 9; 56%) had positive mesenteric lymph node cultures compared with cirrhotics without ascites (0 of 9) and normal controls (0 of 12) ( P E. coli was isolated from both mesenteric lymph nodes and ascites. Rats with cirrhosis and ascites had significantly greater cecal submucosal edema and inflammation than rats with no ascites and controls. Immunoreactivity with E. coli was present in the cecal wall in 3 of 5 animals with E. coli Translocation to mesenteric lymph nodes. Conclusions: In cirrhotic rats, Bacterial Translocation is increased after the development of ascites and may be a major factor in the development of spontaneous infections in cirrhosis.
Bernd Schnabl - One of the best experts on this subject based on the ideXlab platform.
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methods to determine intestinal permeability and Bacterial Translocation during liver disease
Journal of Immunological Methods, 2015Co-Authors: Lirui Wang, Phillipp Hartmann, Cristina Llorente, Peng Chen, Anming Yang, Bernd SchnablAbstract:Liver disease is often times associated with increased intestinal permeability. A disruption of the gut barrier allows microbial products and viable bacteria to translocate from the intestinal lumen to extraintestinal organs. The majority of the venous blood from the intestinal tract is drained into the portal circulation, which is part of the dual hepatic blood supply. The liver is therefore the first organ in the body to encounter not only absorbed nutrients, but also gut-derived bacteria and pathogen associated molecular patterns (PAMPs). Chronic exposure to increased levels of PAMPs has been linked to disease progression during early stages and to infectious complications during late stages of liver disease (cirrhosis). It is therefore important to assess and monitor gut barrier dysfunction during hepatic disease. We review methods to assess intestinal barrier disruption and discuss advantages and disadvantages. We will in particular focus on methods that we have used to measure increased intestinal permeability and Bacterial Translocation in experimental liver disease models.
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Bacterial Translocation and changes in the intestinal microbiome in mouse models of liver disease
Journal of Hepatology, 2012Co-Authors: Derrick E Fouts, David A Brenner, Manolito Torralba, Karen E Nelson, Bernd SchnablAbstract:Background & Aims: Intestinal dysbiosis and Bacterial Translocation are common in patients with advanced liver disease, and there is strong evidence that the Translocation of bacteria and their products across the epithelial barrier drives experimental liver disease progression. The aims of our study were to investigate dynamics of Bacterial Translocation and changes in the enteric microbiome in early stages of liver disease. Methods: Cholestatic liver injury was induced by ligation of the common bile duct (BDL) and toxic liver injury by injection of carbon tetrachloride (CCl4) in mice. Results: Increased intestinal permeability and Bacterial Translocation occurred one day following liver injury in both disease models. This was accompanied by decreased intestinal expression of the tight junction protein occludin. Although BDL resulted in a rapid onset of intestinal Bacterial overgrowth, Bacterial overgrowth was observed in mice injected with CCl4 only in advanced stages of liver fibrosis. To further assess the qualitative changes in the intestinal microbiome, massively parallel pyrosequencing of 16S rRNA genes revealed minor microbial changes following BDL, while CCl4 administration resulted in a relative abundance of Firmicutes and Actinobacteria compared with oil-injected mice. Four different liver disease models (cholestasis, toxic, alcohol, obesity) show few similarities in their intestinal microbiome. Conclusions: Acute liver injury is associated with an early onset of increased intestinal permeability and Bacterial Translocation that precede changes in the microbiome. The enteric microbiome differs with respect to the etiology of liver disease. 2012 European Association for the Study of the Liver. Published
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Bacterial Translocation and changes in the intestinal microbiome associated with alcoholic liver disease
World Journal of Hepatology, 2012Co-Authors: Bernd SchnablAbstract:Alcoholic liver disease progresses through several stages of tissue damage, from simple steatosis to alcoholic hepatitis, fibrosis, or cirrhosis. Alcohol also affects the intestine, increases intestinal permeability and changes the Bacterial microflora. Liver disease severity correlates with levels of systemic Bacterial products in patients, and experimental alcoholic liver disease is dependent on gut derived Bacterial products in mice. Supporting evidence for the importance of Bacterial Translocation comes from animal studies demonstrating that intestinal decontamination is associated with decreased liver fibrogenesis. In addition, mice with a gene mutation or deletion encoding receptors for either Bacterial products or signaling molecules downstream from these receptors, are resistant to alcohol-induced liver disease. Despite this strong association, the exact molecular mechanism of Bacterial Translocation and of how changes in the intestinal microbiome contribute to liver disease progression remains largely unknown. In this review we will summarize evidence for Bacterial Translocation and enteric microbial changes in response to alcoholic liver injury and chronic alcoholic liver disease. We will further describe consequences of intestinal dysbiosis on host biology. We finally discuss how therapeutic interventions may modify the gastrointestinal microflora and prevent or reduce alcoholic liver disease progression.
Yuval Haskel - One of the best experts on this subject based on the ideXlab platform.
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the modulatory role of gut hormones in elemental diet and intravenous total parenteral nutrition induced Bacterial Translocation in rats
Journal of Parenteral and Enteral Nutrition, 1994Co-Authors: Yuval Haskel, Edwin A DeitchAbstract:We have previously shown that parenteral and certain elemental diets promote Bacterial Translocation and that this diet-induced Bacterial Translocation can be prevented by the provision of bulk-forming dietary fiber. The goal of the current study was to test the hypothesis that fiber's protective effect on diet-induced Bacterial Translocation was mediated by trophic gut hormones. This hypothesis was tested by using bombesin (which stimulates gut hormone release) or the somatostatin analog Sandostatin (which inhibits gut hormone release) to modulate gut hormone release in rats receiving rat food, intravenous total parenteral nutrition, or an elemental diet. Both bombesin and fiber were effective in preventing elemental diet-induced Bacterial Translocation, whereas octreotide acetate abrogated the protective effect of fiber. Bombesin was also effective in limiting Bacterial Translocation in parenterally fed rats. Although both enteral (elemental diet) and parenteral diet-induced Bacterial Translocation were...
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elemental diet induced Bacterial Translocation can be hormonally modulated
Annals of Surgery, 1993Co-Authors: Yuval Haskel, Edwin A DeitchAbstract:BACKGROUND: The authors have previously documented that feeding mice an elemental diet resulted in Bacterial Translocation (BT) that could be prevented by the provision of dietary fiber. To test whether the protective effect of fiber was related to the stimulation of trophic gut hormones, the effects of sandostatin and bombesin were tested. METHODS: Mice fed either chow or the elemental diet were stratified into several groups and the ability of bombesin (10 micrograms/kg, tid) or sandostatin (100 micrograms/kg bid) to modulate BT was examined. After 14 days, mice were sacrificed and BT, cecal Bacterial population levels, mucosal protein, and small bowel weight was measured. Segments of the ileum and jejunum were examined histologically. RESULTS: Incidence of elemental diet-induced BT (75%) was reduced by fiber (9%) or the administration of bombesin (13%) (p < 0.01). Although sandostatin did not promote BT in chow-fed mice, it reversed the protective effect of fiber on BT (75%) (p < 0.01). CONCLUSION: Elemental diet-induced Bacterial Translocation can be modulated hormonally and the beneficial effects of fiber on diet-induced BT appears to be hormonally mediated.