• Ross F Goldberg, William G Austen, Xiaobo Zhang, Gitonga Munene, Golam Mostafa, Shaluk Biswas, Michael McCormack, Kyle R Eberlin, John T Nguyen, Hamit S Tatlidede, H Shaw Warren, Sonoko Narisawa, Jose L Millán, and Richard A Hodin.
• Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.
• Proc. Natl. Acad. Sci. U.S.A. 2008 Mar 4; 105 (9): 3551-6.

AbstractUnder 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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