title: Enteral nutrition modifies gut-associated lymphoid tissue in rat regardless of the molecular form of nitrogen supply.
abstract: BACKGROUND
  It has been suggested that beneficial effect of elemental enteral diets in the treatment of inflammatory bowel diseases could be mediated by the suppression of protein dietary antigens. The objective of the present work was to study the effect of enteral diet on gut associated lymphoid tissue and on gastric Lactobacillus flora, in rat.
  
  
  METHODS
  The effects of three molecular forms of nitrogen supply: amino acids, oligopeptides or whole casein, were compared in rats on continuous enteral diet. Frozen sections of small bowel were studied with monoclonal antibodies anti-CD5, -CD4, -CD8, -CD25, -macrophages, -MHC II. The Lactobacillus flora was also enumerated in the stomach, in order to assess the effect of ED on rat flora.
  
  
  RESULTS
  Growth and mucosa morphology were identical in control and enteral groups. Rats on enteral diet showed, whatever was the molecular form of nitrogen supply, a decrease in CD5+, CD4+ and CD8+ intraepithelial cell numbers, but not in lamina propria cell number, and a decreased MHC II epithelial expression, when compared to control rats. The enterally fed rats also showed a decrease in Lactobacillus gastric contents.
  
  
  CONCLUSIONS
  The current study demonstrates that continuous enteral nutrition modifies MHC II epithelial expression and gut associated lymphoid tissue cell number in rat, whatever is the molecular form of nitrogen supply. Intestinal flora could be responsible, at least for part, for these results.
authors.affiliation: Unité d'Ecologie et de Physiologie du Système Digestif, Jouy-En-Josas, France.
authors.forename: G
authors.initials: G
authors.lastname: Guihot
authors.forename: V
authors.initials: V
authors.lastname: Merle
authors.forename: M
authors.initials: M
authors.lastname: Leborgne
authors.forename: G
authors.initials: G
authors.lastname: Pivert
authors.forename: O
authors.initials: O
authors.lastname: Corriol
authors.forename: N
authors.initials: N
authors.lastname: Brousse
authors.forename: C
authors.initials: C
authors.lastname: Ricour
authors.forename: V
authors.initials: V
authors.lastname: Colomb
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology; D015703:Antigens, CD / Q000032:analysis / Q000276:immunology; D015704:CD4 Antigens / Q000032:analysis / Q000276:immunology; D018956:CD5 Antigens / Q000032:analysis / Q000276:immunology; D016827:CD8 Antigens / Q000032:analysis / Q000276:immunology; D015331:Cohort Studies; D015169:Colony Count, Microbial; D004386:Duodenum / Q000276:immunology / Q000502:physiology / Q000648:ultrastructure; D004750:Enteral Nutrition; D004848:Epithelium / Q000276:immunology / Q000502:physiology / Q000648:ultrastructure; D000949:Histocompatibility Antigens Class II / Q000032:analysis / Q000276:immunology; D007150:Immunohistochemistry; D007421:Intestine, Small / Q000276:immunology / Q000502:physiology* / Q000648:ultrastructure; D007583:Jejunum / Q000276:immunology / Q000502:physiology / Q000648:ultrastructure; D007778:Lactobacillus / Q000254:growth & development; D008221:Lymphoid Tissue / Q000276:immunology / Q000502:physiology* / Q000648:ultrastructure; D008871:Microvilli / Q000648:ultrastructure; D051381:Rats; D013270:Stomach / Q000382:microbiology*; D016176:T-Lymphocyte Subsets / Q000166:cytology / Q000276:immunology; D015430:Weight Gain / Q000502:physiology
chemical_list: D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D015704:CD4 Antigens; D018956:CD5 Antigens; D016827:CD8 Antigens; D000949:Histocompatibility Antigens Class II