Intestinal alkaline phosphatase is a gut mucosal defense factor maintained by enteral nutrition

被引:291
作者
Goldberg, Ross F. [1 ]
Austen, William G., Jr. [1 ]
Zhang, Xiaobo [1 ]
Munene, Gitonga [1 ]
Mostafa, Golam [1 ]
Biswas, Shaluk [1 ]
McCormack, Michael [1 ]
Eberlin, Kyle R. [1 ]
Nguyen, John T. [1 ]
Tatlidede, Hamit S. [1 ]
Warren, H. Shaw [2 ]
Narisawa, Sonoko [3 ]
Millan, Jose L. [3 ]
Hodin, Richard A. [1 ]
机构
[1] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Surg, Boston, MA 02114 USA
[2] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Pediat, Boston, MA 02114 USA
[3] Burnham Inst Med Res, La Jolla, CA 92037 USA
关键词
gut barrier; lipopolysaccharide; trophic feeding; bacterial translocation; NF-kappa B;
D O I
10.1073/pnas.0712140105
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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.
引用
收藏
页码:3551 / 3556
页数:6
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