| Abstrakt: |
The gut primes neutrophils PMNs during injury, which can then induce distant organ damage after a second insult. ICAM1 is an important adhesion molecule in PMN attachment to the vascular endothelium. Parenteral nutrition TPN decreases gut levels of interleukin IL4 and IL10, two cytokines that are normal inhibitors of ICAM1 expression. TPN also increases gut ICAM1 expression and PMN accumulation. Since glutamine GLN and bombesin BBS prevent TPNassociated impairment of mucosal immunity, we hypothesized that GLN and BBS would modulate organ ICAM1 expression in association with normalization of IL4 and IL10 levels. Fortyfour mice were fed chow, TPN, or GLNTPN isonitrogenous 2 GLNenriched TPN. After 5 days of diets, ICAM1 expression was quantified in organs using the dual radiolabeled monoclonal antibody technique. In the next experiment, 29 mice were fed chow, TPN, or BBSTPN BBS 15 gkg TID for 5 days to measure organ ICAM1 expression. Total IL4 and IL10 levels were measured with ELISA from intestinal homogenates of another set of 52 mice fed chow, TPN, GLNTPN, or BBSTPN. TPN significantly increased ICAM1 expression in the lung, kidney, and intestine compared with chow mice. GLNTPN decreased intestinal, but not lung, ICAM1 expression, while BBSTPN reduced pulmonary, but not gut, ICAM1 levels. GLN and BBSTPN returned gut IL4 levels to normal, but failed to increase IL10 levels. GLN and BBS had different effects on organ ICAM1 expression induced by lack of enteral nutrition. Mechanisms other than recovery of IL4 alone may be responsible for gut ICAM1 expression. |
