title: Characteristics of the intestinal epithelial barrier during dietary manipulation and glucocorticoid stress.
abstract: OBJECTIVE
  a) To determine the significance of stress-induced alterations in intestinal permeability by measuring the transmucosal flux of formyl-methionyl-leucyl-phenylalanine (f-MLP), a ubiquitous neutrophilic chemoattractant present in the human and rodent colon; and b) to determine whether stress and/or diet influence(s) bacterial adherence-induced changes in epithelial permeability by affecting the production of secretory immunoglobulin A (IgA), the main immune mechanism preventing bacterial adherence.
  
  
  METHODS
  Prospective, randomized, controlled study.
  
  
  METHODS
  University animal research laboratory.
  
  
  METHODS
  Female Fischer rats.
  
  
  METHODS
  Rats were randomly assigned to four groups of seven animals each. Groups of animals were assigned to receive saline or dexamethasone (0.8 mg/kg ip) and were either starved (5% dextrose in water ad libitum) or fed (water and rat chow) for 48 hrs.
  
  
  RESULTS
  Mucosal barrier function was evaluated by measuring secretory IgA, bacterial adherence to the intestinal mucosa, and transepithelial electrical resistance, a measure of tight junction permeability. The f-MLP permeation across the mucosa was also determined in segments with significant permeability changes. Results indicate that starvation in dexamethasone-treated rats significantly impairs secretory IgA, promotes bacterial adherence to the mucosa, and results in increased intestinal permeability to f-MLP. These effects are significantly attenuated by the feeding of rat chow.
  
  
  CONCLUSIONS
  Alterations in intestinal barrier function are characterized by depressed IgA, bacterial adherence to the intestinal mucosa, and permeation of clinically relevant proinflammatory luminal macromolecules (f-MLP). Enteral stimulation with foodstuffs is a necessary protective measure to prevent altered epithelial barrier function during glucocorticoid stress.
authors.affiliation: Department of Surgery, University of Illinois, Chicago, USA.
authors.forename: J C
authors.initials: JC
authors.lastname: Spitz
authors.forename: S
authors.initials: S
authors.lastname: Ghandi
authors.forename: M
authors.initials: M
authors.lastname: Taveras
authors.forename: E
authors.initials: E
authors.lastname: Aoys
authors.forename: J C
authors.initials: JC
authors.lastname: Alverdy
mesh_terms: D000818:Animals; D001422:Bacterial Adhesion / Q000502:physiology; D002463:Cell Membrane Permeability / Q000502:physiology; D002630:Chemotactic Factors / Q000493:pharmacokinetics; D003907:Dexamethasone / Q000494:pharmacology*; D004032:Diet; D004848:Epithelium / Q000502:physiology; D005260:Female; D005938:Glucocorticoids / Q000494:pharmacology*; D007071:Immunoglobulin A, Secretory / Q000032:analysis; D007413:Intestinal Mucosa / Q000502:physiology; D007420:Intestine, Large / Q000502:physiology*; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000493:pharmacokinetics; D011446:Prospective Studies; D011897:Random Allocation; D051381:Rats; D013217:Starvation / Q000503:physiopathology; D013312:Stress, Physiological / Q000503:physiopathology*
chemical_list: D002630:Chemotactic Factors; D005938:Glucocorticoids; D007071:Immunoglobulin A, Secretory; D009240:N-Formylmethionine Leucyl-Phenylalanine; D003907:Dexamethasone