Route of nutrition influences intercellular adhesion molecule-1 expressionand neutrophil accumulation in intestine

Hypothesis: The levels of intestinal interleukin 10 and interleukin 4, inhi bitors of intercellular adhesion molecule-1 (ICAM-1) expression, decline wi th total parenteral nutrition (TPN). These cytokine changes induced by lack of enteral nutrition may increase ICAM-1 expression, resulting in polymorp honuclear neutrophil accumulation in intestine. Design: Prospective randomized experimental trials. Setting: Laboratory. Materials: Male mice. Interventions: Sixty-three mice were randomized to chow, intravenous TPN, o r intragastric TPN. Main Outcome Measures: Experiment 1: After diet manipulation, iodine 125-la beled anti-ICAM-1 antibody and iodine 131-labeled nonbinding antibody were injected to quantify ICAM-1 expression on endothelial cells in the lung, li ver, kidney, and small intestine. Measurement of myeloperoxidase was used t o quantify polymorphonuclear neutrophil accumulation in the organs. Experim ent 2. Intestine was harvested for bo th ICAM-1 and myeloperoxidase levels after chow refeeding of mice in the intravenous TPN group. Results: In experiment 1, uninjured mice fed intravenous TPN showed signifi cantly increased intestinal ICAM-1 expression and polymorphonuclear neutrop hil accumulation with no significant changes in the lung, liver, or kidney. No changes occurred in mice fed chow or intragastric TPN. In experiment 2, reinstitution of enteral feeding returned intestinal ICAM-1 and myeloperox idase levels to normal. Conclusion: Gut changes associated with lack of enteral feeding induce endo thelial changes and an immunologic response, which may influence subsequent responses to injury.