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Enteral Feeding Decreases Gut Apoptosis, Permeability, And Lung Inflammation During Murine Endotoxemia

Kurt T. Alscher, P. Terry Phang, Treena E. McDonald, Keith R. Walley

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We tested the hypothesis that endotoxemia and fasting are associated with increased gut apoptotic activity, gut permeability, and inflammation in a distant organ. Fed or fasted CD-1 mice were studied 6 h after intraperitoneal injection of either saline (sham) or endotoxin (4 mg/kg of 0111:B4 Escherichia coli lipopolysaccharide). We found that endotoxin increased gut caspase-3 and -6 activity by 4.9 ± 0.6- and 4.5 ± 0.5-fold, respectively ( P < 0.001), and increased terminal deoxynucleotidyltransferase-mediated dUTP nick-end labeling (TUNEL) staining of mucosal cells ( P< 0.05). Feeding decreased caspase-3 activity by 40% ( P< 0.05) and decreased endotoxin-induced TUNEL staining ( P< 0.05). Endotoxin increased gut poly(ADP-ribose) polymerase activity by 15% ( P < 0.05). Endotoxin increased gut permeability by 44% ( P < 0.05), an effect reduced 36% by feeding ( P < 0.05). Similarly, endotoxin increased pulmonary neutrophil infiltration (6.0 ± 1.0-fold, P< 0.001) and increased lung interleukin (IL)-6 (5.9 ± 0.1-fold, P < 0.001) and macrophage inflammatory protein (MIP)-2 expression (290 ± 40-fold, P < 0.001), whereas feeding decreased this effect by 43% for neutrophils, 40% for IL-6 ( P < 0.05), and 35% for MIP-2 ( P < 0.05). Thus endotoxin increases gut apoptotic activity, gut permeability, and pulmonary inflammation. Enteral feeding may decrease the distant organ inflammation by reducing gut apoptosis, thereby maintaining gut mucosal function during endotoxemia.