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Probiotics upregulate MUC-2 mucin gene expression in a Caco-2 cell-culture model
INTERNATIONAL ABSTRACTS
a quick and easy technical adaptation of Soave’s method with excellent results especially in babies. Critical issues mentioned by the authors are (1) that the best level of mucosal dissection to preserve delicate nerve endings for sensation and continence is unclear, (2) that the pullthrough of very large megacolon in older children causes marked anorectal distension probably followed by temporary soiling, and (3) that the technique is useful for rectosigmoid aganglionosis only and should not be used in unclear extension without reliable evaluation by biopsies.—Peter Schmittenbecher Probiotics Upregulate MUC-2 Mucin Gene Expression in a Caco-2 Cell-Culture Model. A.F. Mattar, D.H Teiltelbaum, R.A. Drongowski,et al. Pediatr Surg Int 18:586-589, (October), 2002. Probiotics are expected to enhance the intestinal microflora and inhibit growth of pathogenic flora. Lactobacillus casei (LC) adheres to surface receptors of cultured enterocytes and inhibits bacterial translocation. The authors hypothesized that LC-mediated inhibition of bacterial translocation is controlled by an upregulation of epithelial mucin MUC-2. LC in a concentration of 104 up to 108 colony-forming units per milliliter were placed on a culture of human colon carcinoma (Caco-2) cells. Translocation of Escherichi coli isolated from a newborn with necrotizing enterocolitis and prepared at a concentration of 105 colony-forming units per milliliter, across the Caco-2 monolayer was measured, and anti–MUC-2 antibody signal expression quantified by densitometry and mRNA by spectrophotometry. E coli translocation across Caco-2 monolayer was reduced by LC dose-dependent from 21.7% up to complete inhibition in the highest LC concentration. MUC-2 expression was elevated significantly by factor 8.6 and 15.6 in the low- and high-dose LC groups, respectively. Even MUC-2 mRNA was 50% higher after LC application. Probiotics enhance intestinal microflora and show further beneficial effects by reduction of gut luminal pH, direct antagonistic effects on pathogens, competition for binding and receptor sites, and improving immune function. The experiments showed that the inhibition of translocation of enteropathogen E coli takes place by LC-induced dose-dependent upregulation of MUC-2 mucin expression. Because the use of nonpathogenic bacteria as probiotics is safe even in immunocompromised patients, the risk of probiotics usage in a clinical setting appears small.—Peter Schmittenbecher The Role of Contractile Microfilaments in the Morphogenesis of the Developing Foregut of Chick Embryos. S. Hosie, M. Farag, M. Vena, et al. Pediatr Surg Int 18:611-614, (October), 2003. In early embryonic stages, the foregut is a tubular structure consisting of endodermal cells. The cell shape is stabilized by an internal filamentous framework called cytoskeleton. Contractile microfilaments can change cell and tissue shape. The aim of this study was to clarify the role of these filaments during foregut morphogenesis. Fertile white leghorn eggs between stage 14 and 24 (2- to 4-day-old embryos) were exposed to cytochalasin D (CD). Immunofluorescent staining with phalloidin, which specifically binds to actin filaments, imaged a bright, regular, evenly distributed fluorescent band at the luminal side of the cylindrical epithelial cells in sections of control eggs. CD-treated embryos lacked this band. After microdissection, control embryos showed a foregut with a smooth, regular cylindrical structure, narrow and straight lumen with ventral and dorsal walls in close apposition. CD-treated specimen showed a wide foregut lumen, separated walls, and an atonic structure without straight tubular configuration. Contractile microfilaments take part in morphogenesis of different organs and structures. Inhibition of actin is followed by loss of shape. In the foregut development, even the tonus of the organ is lost. The long-term
1123
effect of this disturbance of cytoskeleton remains unclear, because CD kills the embryos immediately, but morphogenesis runs over longer time. Therefore, further studies are necessary to fully understand the observed structural changes in this momentary view.—Peter Schmittenbecher Liposaccharide Endotoxemia Reduces Cell Proliferation and Decreases Enterocyte Apoptosis During Intestinal Adaptation in a Rat Model of Short-Bowel Syndrome. I. Sukhotnik, E. Yakirevich, A.G. Coran, et al. Pediatr Surg Int 18:615-619, (October), 2002. After massive small bowel resection, cellular hyperplasia leads to increased villus height and crypt depth and, therefore, to marked increase of the intestinal cell-surface area. Sepsis is a well-known complication in short-bowel patients. The authors asked whether sepsis impedes intestinal adaptation and contributes to gastrointestinal dysfunction. In male Sprangue-Dawley rats, sham-operated animals (ileum transection and anastomosis without resection) were compared with short bowel syndrome (SBS) rats (75% mid small bowel resection with or without application of 10 mg/kg/d lipopolysaccharides (LPS). 15 days later, 3 segments (duodenum, small bowel up to anastomosis, terminal ileum) were calculated according total bowel weight, weight per centimeter bowel length, mucosal weight, DNA and protein concentration per centimeter bowel length. Villus height and crypt depth was measured and proliferation index and apoptosis index calculated based on special immunhistochemical staining. SBS rats had a significant loss of body weight, a marked increase in bowel and mucosal weight per centimeter in all 3 segments, a significant increase in DNA as well as in total protein in the jejunum and ileum segments, a 23% to 54% increase in crypt depth and villus height, an elevated proliferation index, and even an increase in ileal apoptosis as a sign of cell turnover compared with the sham-operated group. LPS administration resulted in decreased bowel and mucosal weight, in a decrease of DNA and total ileal protein content, in a loss of villus height and crypt depth, and in an decreased proliferation and ileal apoptosis index compared with SBS alone. LPS endotoxemia affects intestinal adaptation: it inhibits mucosal regrowth and reduces enterocyte turnover.—Peter Schmittenbecher
ABDOMEN Treatment of Transient Posttraumatic Bile-Duct Stenosis by Laparoscopic-Assisted Cholecystotomy. R.B Tro¨ bs, W. Siekmeyer, U. Bu¨ hligen, et al. J. Pediatr Surg Int 18:503-504, (September), 2002. An isolated blunt injury to the extrahepatic bile ducts is rare. The authors report on a 10-year-old boy with marked jaundice 3 weeks after blunt trauma with an enlarged liver, abnormal liver function tests, a hydropic gallblader, and dilated common bile duct. The pancreas appeared normal by ultrasound scan. Endoscopic retrograde and magnetic resonance cholangiographies showed a distal common bile duct stenosis with prestenotic dilatation. Because a posttraumatic obstructing edema was highly probable, they inserted a 5F catheter by a laparoscopic-assisted procedure and diverted 1,500 mL bile volume daily. Two weeks later, a cholangiogram via the tube showed satisfactory passage of contrast to the duodenum so that the tube was clamped and removed 2 weeks later. The boy has remained free of symptoms. Surgical options for extrahepatic bile-duct stenosis include percutaneous transhepatic drainage (PTD), placement of indwelling stents, placement of a cholecystotomy tube, and cholecystoenterostomy or choledochojejunostomy. If biliary obstruction is expected to be temporary, then a temporary procedure should be used. Laparoscopic-assisted cholecystotomy represents a safe and effective method with the opportunity of external cholecystoenteric bypass of bile via a gastroduodenal
a quick and easy technical adaptation of Soave’s method with excellent results especially in babies. Critical issues mentioned by the authors are (1) that the best level of mucosal dissection to preserve delicate nerve endings for sensation and continence is unclear, (2) that the pullthrough of very large megacolon in older children causes marked anorectal distension probably followed by temporary soiling, and (3) that the technique is useful for rectosigmoid aganglionosis only and should not be used in unclear extension without reliable evaluation by biopsies.—Peter Schmittenbecher Probiotics Upregulate MUC-2 Mucin Gene Expression in a Caco-2 Cell-Culture Model. A.F. Mattar, D.H Teiltelbaum, R.A. Drongowski,et al. Pediatr Surg Int 18:586-589, (October), 2002. Probiotics are expected to enhance the intestinal microflora and inhibit growth of pathogenic flora. Lactobacillus casei (LC) adheres to surface receptors of cultured enterocytes and inhibits bacterial translocation. The authors hypothesized that LC-mediated inhibition of bacterial translocation is controlled by an upregulation of epithelial mucin MUC-2. LC in a concentration of 104 up to 108 colony-forming units per milliliter were placed on a culture of human colon carcinoma (Caco-2) cells. Translocation of Escherichi coli isolated from a newborn with necrotizing enterocolitis and prepared at a concentration of 105 colony-forming units per milliliter, across the Caco-2 monolayer was measured, and anti–MUC-2 antibody signal expression quantified by densitometry and mRNA by spectrophotometry. E coli translocation across Caco-2 monolayer was reduced by LC dose-dependent from 21.7% up to complete inhibition in the highest LC concentration. MUC-2 expression was elevated significantly by factor 8.6 and 15.6 in the low- and high-dose LC groups, respectively. Even MUC-2 mRNA was 50% higher after LC application. Probiotics enhance intestinal microflora and show further beneficial effects by reduction of gut luminal pH, direct antagonistic effects on pathogens, competition for binding and receptor sites, and improving immune function. The experiments showed that the inhibition of translocation of enteropathogen E coli takes place by LC-induced dose-dependent upregulation of MUC-2 mucin expression. Because the use of nonpathogenic bacteria as probiotics is safe even in immunocompromised patients, the risk of probiotics usage in a clinical setting appears small.—Peter Schmittenbecher The Role of Contractile Microfilaments in the Morphogenesis of the Developing Foregut of Chick Embryos. S. Hosie, M. Farag, M. Vena, et al. Pediatr Surg Int 18:611-614, (October), 2003. In early embryonic stages, the foregut is a tubular structure consisting of endodermal cells. The cell shape is stabilized by an internal filamentous framework called cytoskeleton. Contractile microfilaments can change cell and tissue shape. The aim of this study was to clarify the role of these filaments during foregut morphogenesis. Fertile white leghorn eggs between stage 14 and 24 (2- to 4-day-old embryos) were exposed to cytochalasin D (CD). Immunofluorescent staining with phalloidin, which specifically binds to actin filaments, imaged a bright, regular, evenly distributed fluorescent band at the luminal side of the cylindrical epithelial cells in sections of control eggs. CD-treated embryos lacked this band. After microdissection, control embryos showed a foregut with a smooth, regular cylindrical structure, narrow and straight lumen with ventral and dorsal walls in close apposition. CD-treated specimen showed a wide foregut lumen, separated walls, and an atonic structure without straight tubular configuration. Contractile microfilaments take part in morphogenesis of different organs and structures. Inhibition of actin is followed by loss of shape. In the foregut development, even the tonus of the organ is lost. The long-term
1123
effect of this disturbance of cytoskeleton remains unclear, because CD kills the embryos immediately, but morphogenesis runs over longer time. Therefore, further studies are necessary to fully understand the observed structural changes in this momentary view.—Peter Schmittenbecher Liposaccharide Endotoxemia Reduces Cell Proliferation and Decreases Enterocyte Apoptosis During Intestinal Adaptation in a Rat Model of Short-Bowel Syndrome. I. Sukhotnik, E. Yakirevich, A.G. Coran, et al. Pediatr Surg Int 18:615-619, (October), 2002. After massive small bowel resection, cellular hyperplasia leads to increased villus height and crypt depth and, therefore, to marked increase of the intestinal cell-surface area. Sepsis is a well-known complication in short-bowel patients. The authors asked whether sepsis impedes intestinal adaptation and contributes to gastrointestinal dysfunction. In male Sprangue-Dawley rats, sham-operated animals (ileum transection and anastomosis without resection) were compared with short bowel syndrome (SBS) rats (75% mid small bowel resection with or without application of 10 mg/kg/d lipopolysaccharides (LPS). 15 days later, 3 segments (duodenum, small bowel up to anastomosis, terminal ileum) were calculated according total bowel weight, weight per centimeter bowel length, mucosal weight, DNA and protein concentration per centimeter bowel length. Villus height and crypt depth was measured and proliferation index and apoptosis index calculated based on special immunhistochemical staining. SBS rats had a significant loss of body weight, a marked increase in bowel and mucosal weight per centimeter in all 3 segments, a significant increase in DNA as well as in total protein in the jejunum and ileum segments, a 23% to 54% increase in crypt depth and villus height, an elevated proliferation index, and even an increase in ileal apoptosis as a sign of cell turnover compared with the sham-operated group. LPS administration resulted in decreased bowel and mucosal weight, in a decrease of DNA and total ileal protein content, in a loss of villus height and crypt depth, and in an decreased proliferation and ileal apoptosis index compared with SBS alone. LPS endotoxemia affects intestinal adaptation: it inhibits mucosal regrowth and reduces enterocyte turnover.—Peter Schmittenbecher
ABDOMEN Treatment of Transient Posttraumatic Bile-Duct Stenosis by Laparoscopic-Assisted Cholecystotomy. R.B Tro¨ bs, W. Siekmeyer, U. Bu¨ hligen, et al. J. Pediatr Surg Int 18:503-504, (September), 2002. An isolated blunt injury to the extrahepatic bile ducts is rare. The authors report on a 10-year-old boy with marked jaundice 3 weeks after blunt trauma with an enlarged liver, abnormal liver function tests, a hydropic gallblader, and dilated common bile duct. The pancreas appeared normal by ultrasound scan. Endoscopic retrograde and magnetic resonance cholangiographies showed a distal common bile duct stenosis with prestenotic dilatation. Because a posttraumatic obstructing edema was highly probable, they inserted a 5F catheter by a laparoscopic-assisted procedure and diverted 1,500 mL bile volume daily. Two weeks later, a cholangiogram via the tube showed satisfactory passage of contrast to the duodenum so that the tube was clamped and removed 2 weeks later. The boy has remained free of symptoms. Surgical options for extrahepatic bile-duct stenosis include percutaneous transhepatic drainage (PTD), placement of indwelling stents, placement of a cholecystotomy tube, and cholecystoenterostomy or choledochojejunostomy. If biliary obstruction is expected to be temporary, then a temporary procedure should be used. Laparoscopic-assisted cholecystotomy represents a safe and effective method with the opportunity of external cholecystoenteric bypass of bile via a gastroduodenal