Abstracts
1998 Digestive Disease Week

#2705

GLUTAMINE PREVENTS LPS-INDUCED NF-_B ACTIVATION IN HUMAN INTESTINAL EPITHELIAL CELLS. MR Moon, TA Pritts, AL Salzman, JE Fischer, and PO Hasselgren. Department of Surgery, University of Cincinnati Medical Center, Children's Hospital Medical Center, and Shriners Burn Institute. Cincinnati, Ohio.

Glutamine (GLN) is an essential fuel utilized by the enterocyte and is crucial in the protection and growth of intestinal mucosa. Recent studies suggest that endotoxemia is associated with decreased enterocyte GLN uptake. Other studies have shown that endotoxemia may be associated with activation of the inflammatory transcription factor NF-_B in the intestinal mucosa. The role of glutamine depletion in endotoxin-induced NF-_B activation is not known. We tested the hypothesis that GLN prevents LPS-induced NF-_B activation in intestinal epithelial cells. Methods: Caco-2 cells, a human intestinal epithelial cell line, were grown to 90% confluence in the presence or absence of glutamine (6mM) for 6 days, then treated with various concentrations of LPS (1-20 µg/ml). After 2 h, cell nuclei were harvested for analysis of NF-_B activity by electrophoretic mobility shift assay (EMSA). Results: NF-_B was activated by LPS in cells cultured in GLN-free medium (Fig. 1, lanes 5-7) but not in cells cultured in the presence of GLN (lanes 1-4).

Conclusions: The results suggest that GLN prevents LPS-induced NF-_B activation in the enterocyte. The protective effect of GLN on intestinal mucosa may at least in part reflect a downregulated inflammatory response in the enterocyte.

Copyright 1996 - 1998, SSAT, Inc. Revised 29 June 1998.