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

The gut primes neutrophils (PMNs) during injury, which can then induce dist ant organ damage after a second insult. ICAM-1 is an important adhesion mol ecule in PMN attachment to the vascular endothelium. Parenteral nutrition ( TPN) decreases gut levels of interleukin (IL)-4 and IL-10, two cytokines th at 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 tha t GLN and BBS would modulate organ ICAM-1 expression in association with no rmalization of IL-4 and IL-10 levels. Forty-four mice were fed chow, TPN, o r GLN-TPN (isonitrogenous 2% GLN-enriched TPN). After 5 days of diets, ICAM -1 expression was quantified in organs using the dual radiolabeled monoclon al antibody technique. In the next experiment, 29 mice were fed chow, TPN, or BBS-TPN (BBS 15 mug/kg TID) for 5 days to measure organ ICAM-1 expressio n. Total IL-4 and IL-10 levels were measured with ELISA from intestinal hom ogenates 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 intestin e 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 increas e IL-10 levels. GLN and BBS had different effects on organ ICAM-1 expressio n induced by lack of enteral nutrition. Mechanisms other than recovery of I L-4 alone may be responsible for gut ICAM-1 expression.