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Enteral feeding decreases gut apoptosis, gut permeability, and pulmonary inflammation during murine endotoxemia Alscher, Kurt Thomas


Background: The systemic response to sepsis is associated with gut mucosal damage, increased permeability, and subsequently increased inflammation in distant organs. Enteral feeding may reduce mortality from multiple organ failure by maintaining the gut mucosal barrier, however the mechanism of this is unclear. We tested the hypothesis that endotoxemia is associated with increased gut apoptosis, increased gut permeability, and increased pulmonary inflammation. Furthermore, we postulate that enteral feeding ameliorates endotoxin's effect on these parameters. Methods: Four groups of 10 male CD-1 mice were studied: fed/sham, fasted/sham, fed/endotoxemic, fasted/endotoxemic. Fasted mice were denied food for 16 hours prior to injection of either saline or E. coli endotoxin. Fed animals received rodent chow throughout. Six hours post injection the gut and lungs were removed and frozen. We assessed gut apoptosis by measuring gut caspase 3, caspase 6 and PARP enzymatic activity. Gut permeability was quantified by measuring the transfer of fluorescein labeled dextran (FD-4) across the gut wall, and pulmonary inflammation was quantified by lung interleukin 6 (IL-6) and macrophage inflammatory protein-2 (MIP-2) ELISA. Results: 1) Apoptosis - After LPS injection, gut caspase 3 and 6 activity increased by 4.9 fold and 4.5 fold respectively (p

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