Modulation of organ ICAM-1 expression during IV-TPN with glutamine and bombesin

• Published in: Shock (Augusta, Ga.) Ga.), 2001-01, Vol.15 (1), p.24-28
• Main Authors: Fukatsu, K, Lundberg, A H, Kudsk, K A, Hanna, M K, Johnson, C D, Wu, Y, Wilcox, H G, Zarzaur, B L
• Format: Article
• Language: English
• Subjects: Animals; Body Weight - drug effects; Bombesin - pharmacology; Glutamine - pharmacology; Intercellular Adhesion Molecule-1 - drug effects; Intercellular Adhesion Molecule-1 - metabolism; Interleukin-10 - metabolism; Interleukin-4 - metabolism; Intestines - drug effects; Intestines - metabolism; Kidney - drug effects; Kidney - metabolism; Liver - drug effects; Liver - metabolism; Male; Mice; Mice, Inbred ICR; Muscle, Skeletal - drug effects; Muscle, Skeletal - metabolism; Parenteral Nutrition
• ISSN: 1073-2322
• DOI: 10.1097/00024382-200115010-00004

The gut primes neutrophils (PMNs) during injury, which can then induce distant organ damage after a second insult. ICAM-1 is an important adhesion molecule in PMN attachment to the vascular endothelium. Parenteral nutrition (TPN) decreases gut levels of interleukin (IL)-4 and IL-10, two cytokines that are normal inhibitors of ICAM-1 expression. TPN also increases gut ICAM-1 expression and PMN accumulation. Since glutamine (GLN) and bombesin (BBS) prevent TPN-associated impairment of mucosal immunity, we hypothesized that GLN and BBS would modulate organ ICAM-1 expression in association with normalization of IL-4 and IL-10 levels. Forty-four mice were fed chow, TPN, or GLN-TPN (isonitrogenous 2% GLN-enriched TPN). After 5 days of diets, ICAM-1 expression was quantified in organs using the dual radiolabeled monoclonal antibody technique. In the next experiment, 29 mice were fed chow, TPN, or BBS-TPN (BBS 15 microg/kg TID) for 5 days to measure organ ICAM-1 expression. Total IL-4 and IL-10 levels were measured with ELISA from intestinal homogenates of another set of 52 mice fed chow, TPN, GLN-TPN, or BBS-TPN. TPN significantly increased ICAM-1 expression in the lung, kidney, and intestine compared with chow mice. GLN-TPN decreased intestinal, but not lung, ICAM-1 expression, while BBS-TPN reduced pulmonary, but not gut, ICAM-1 levels. GLN- and BBS-TPN returned gut IL-4 levels to normal, but failed to increase IL-10 levels. GLN and BBS had different effects on organ ICAM-1 expression induced by lack of enteral nutrition. Mechanisms other than recovery of IL-4 alone may be responsible for gut ICAM-1 expression.