Route of Nutrition Influences Intercellular Adhesion Molecule-1 Expression and Neutrophil Accumulation in Intestine

Abstract

Hypothesis:The levels of intestinal interleukin 10 and interleukin 4, inhibitors of intercellular adhesion molecule-1 (ICAM-1) expression, decline with total parenteral nutrition (TPN). These cytokine changes induced by lack of enteral nutrition may increase ICAM-1 expression, resulting in polymorphonuclear neutrophil accumulation in intestine.Design: Prospective randomized experimental trials. Setting: Laboratory.Materials: Male mice.Interventions: Sixty-three mice were randomized to chow, intravenous TPN, or intragastric TPN. Main Outcome Measures: Experiment 1: After diet manipulation, iodine 125-labeled anti-ICAM-1 antibody and iodine 131-labeled nonbinding antibody were injected to quantify ICAM-1 expression on endothelial cells in the lung, liver, kidney, and small intestine. Mea-surement of myeloperoxidase was used to quantify polymorphonuclear neutrophil accumulation in the organs. Experiment 2: Intestine was harvested for both 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 significantly increased intestinal ICAM-1 expression and polymorphonuclear neutrophil 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 myeloperoxidase levels to normal.Conclusion: Gut changes associated with lack of enteral feeding induce endothelial changes and an immunologic response, which may influence subsequent responses to injury.

Parenteral Nutrition Induces Organ Specific Alterations in Polymeric Immunoglobulin Receptor Levels

“…In studies of severely injured trauma patients, individuals randomized to enteral feeding sustained significantly fewer pneumonias and intraabdominal abscesses than an injured group fed parenterally [15,[20][21][22]. Experimentally, our work and that of others show that route and type of nutrition influence established mucosal immunologic defenses [13,16], intraperitoneal cytokine and immunologic responses [18], and systemic inflammatory responses to injury [6][7][8]. This work focuses on PN induced alterations in mucosal immunity.…”

Total parenteral nutrition adversely affects gut barrier function in neonatal piglets

“…TPN not only reduces the population of enterocytes but also has been associated with expansion of mucosal goblet cells (GCs) and some lymphocyte subtypes (11,30). Furthermore, newborn (11,19) and adult (17) animal studies indicate that TPN-induced activation of lymphocytes may induce mucosal inflammation on the basis of increased ICAM-1 expression and myeloperoxidase activity. Studies in TPN-fed mice demonstrated that increased expression of the proinflammatory cytokine INF-␥ in activated intraepithelial lymphocytes (IELs) is linked to increased apoptosis and may contribute to the breakdown of epithelial barrier integrity (26,63).…”

Critical Care Nutrition: Getting Involved as a Gastrointestinal Endoscopist

“…18,25 In contrast, in a setting of gut disuse, the same dendritic macrophage samples or ''senses'' bacterial overgrowth of pathogenic bacteria and an absence of food antigen present, and as a result interleukin-12 is released. 25,26 After the sampling of the luminal contents, the dendritic macrophage migrates back down into the lamina propria where there is a bed of naive CD-4 helper T-lymphocytes 18 ( Fig. 3).…”

“…29 In contrast, GALT cells which are homing back to the gut to provide protection against luminal bacteria require the expression of mucosal addressin cellular adhesion molecule to pass out of the vascular space and into the lamina propria of the gut. 10,26 With gut disuse and decreases in the T H 2 cytokines, there is down-regulation of mucosal addressin cellular adhesion molecule levels, an effect which essentially closes the door to these GALT cells and prevents their exiting from the vascular space. 10,26 The impact of these physiologic processes is well documented in clinical studies.…”

“…10,26 With gut disuse and decreases in the T H 2 cytokines, there is down-regulation of mucosal addressin cellular adhesion molecule levels, an effect which essentially closes the door to these GALT cells and prevents their exiting from the vascular space. 10,26 The impact of these physiologic processes is well documented in clinical studies. The differential effect of feeding versus starvation on level of oxidative stress is demonstrated in a study by Fong 30 in normal, healthy volunteers.…”