title: Epithelial permeability is not increased in rats following small bowel resection.
abstract: BACKGROUND
  Increased intestinal permeability and translocation of bacteria and/or bacterial products may cause infection and liver dysfunction in patients with the short bowel syndrome. In previous studies, serum from mice undergoing small bowel resection (SBR) enhanced growth of cultured rat intestinal epithelial cells (RIEC-6), implicating a role for a serum factor(s) in the enterocyte response to SBR. These experiments tested the hypothesis that epithelial cell permeability is increased following SBR.
  
  
  METHODS
  Male Sprague-Dawley rats underwent a 75% SBR or sham operation. Intestinal permeability in the remnant ileum was determined by Ussing chambers on Postoperative Day (POD) 3. Additionally, serum was collected on POD 1, 3, and 7 and mesenteric lymph was harvested on POD 3. Once confluent, RIEC-6 cells were incubated for 3 days in media supplemented with 10% fetal bovine serum (FBS; control), 1% FBS, 1% FBS plus 9% Sham serum, or 1% FBS plus 9% SBR serum or exposed to media with varied concentrations of SBR or Sham lymph. Monolayer permeability was determined by measuring the passage of dextran-rhodamine.
  
  
  RESULTS
  Intestinal permeability was reduced in rats undergoing SBR. Sham serum-treated monolayers demonstrated the greatest permeability. Incubation with SBR serum reduced permeability to near control media. There were no permeability differences between SBR and Sham lymph-treated monolayers.
  
  
  CONCLUSIONS
  The early adaptive response of the remnant intestine after SBR is associated with reduced permeability. These results suggest an alternative mechanism for the increased bacterial translocation that has been described following SBR.
authors.affiliation: Division of Pediatric Surgery, Children's Hospital Medical Center, Cincinnati, Ohio, USA.
authors.forename: D P
authors.initials: DP
authors.lastname: O'Brien
authors.forename: L A
authors.initials: LA
authors.lastname: Nelson
authors.forename: L E
authors.initials: LE
authors.lastname: Stern
authors.forename: J L
authors.initials: JL
authors.lastname: Williams
authors.forename: C J
authors.initials: CJ
authors.lastname: Kemp
authors.forename: Q
authors.initials: Q
authors.lastname: Wang
authors.forename: P
authors.initials: P
authors.lastname: Tso
authors.forename: C R
authors.initials: CR
authors.lastname: Erwin
authors.forename: P O
authors.initials: PO
authors.lastname: Hasselgren
authors.forename: B W
authors.initials: BW
authors.lastname: Warner
mesh_terms: D000220:Adaptation, Biological; D000818:Animals; D002460:Cell Line; D002463:Cell Membrane Permeability; D017077:Culture Media, Conditioned; D046508:Culture Techniques; D003911:Dextrans / Q000378:metabolism; D007082:Ileum / Q000254:growth & development / Q000503:physiopathology; D007413:Intestinal Mucosa / Q000503:physiopathology*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D012235:Rhodamines / Q000378:metabolism; D012778:Short Bowel Syndrome / Q000503:physiopathology*
chemical_list: D017077:Culture Media, Conditioned; D003911:Dextrans; D012235:Rhodamines; C051311:rhodamine dextran