Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 105, Issue 9, Pages 3551-3556Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0712140105
Keywords
gut barrier; lipopolysaccharide; trophic feeding; bacterial translocation; NF-kappa B
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Funding
- NIDDK NIH HHS [DK50623, DK47186, R01 DK047186, R01 DK050623] Funding Source: Medline
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Under conditions of starvation and disease, the gut barrier becomes impaired, and trophic feeding to prevent gut mucosal atrophy has become a standard treatment of critically ill patients. However, the mechanisms responsible for the beneficial effects of enteral nutrition have remained a mystery. Using in vitro and in vivo models, we demonstrate that the brush-border enzyme, intestinal alkaline phosphatase (IAP), has the ability to detoxify lipopolysaccharide and prevent bacterial invasion across the gut mucosal barrier. IAP expression and function are lost with starvation and maintained by enteral feeding. It is likely that the IAP silencing that occurs during starvation is a key component of the gut mucosal barrier dysfunction seen in critically ill patients.
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