Enteral Nutrition Modifies Gut‐associated Lymphoid Tissue in Rat Regardless of the Molecular Form of Nitrogen Supply

Author:

Guihot Gwénaële12,Merle Véronique2,Leborgne Michelle2,Pivert Gérard2,Corriol Odile3,Brousse Nicole2,Ricour Claude4,Colomb Virginie4

Affiliation:

1. Unité d'Ecologie et de Physiologie du Système Digestif Jouy‐En‐Josas

2. Service d'Anatomopathologie Hôpital Necker‐Enfants Malades Paris

3. Pharmacie Hôpital Necker‐Enfants Malades Paris

4. Service de Gastroentérologie et Nutrition Pédiatriques Hôpital Necker‐Enfants Malades Paris France

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: aminoacids, 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.

Publisher

Wiley

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