Ramasamy S, Nguyen DD, Eston MA et al. Inflamm Bowel Dis 2011;17:532–42.
Intestinal alkaline phosphatase (IAP) is a small-intestinal brush border enzyme that functions as a gut mucosal defense factor. In this study, Ramasamy and colleagues demonstrated that orally administered calf IAP is protective in two chronic colitis models, one in which colitis was induced by dextran sodium sulfate and another in which radiation was applied to Wiskott–Aldrich Sydrome Protein-deficient mice.
The maintenance of normal host–microbial interaction includes epithelial barrier function conferred by host factors such as antimicrobial peptides (e.g. defensins). The dysregulation of such factors influences the microbial composition and subsequent host immune response, and is considered to be important in the pathogenesis of IBD. Intestinal alkaline phosphatase (IAP) is of significant interest as it has the ability to detoxify bacterial lipopolysaccharide (LPS) from Gram-negative bacteria, and exogenous IAP has been shown to attenuate LPS-mediated toxicity [1]. Intestinal IAP expression is reduced in IBD and exogenous administration of IAP in a rat dextran sodium sulfate (DSS)-induced acute colitis model has been shown to be protective [2]. Ramasamy et al. further confirmed this in two chronic models using either repeated cycles of DSS challenge or sublethal radiation damage to Wiskott–Aldrich Sydrome Protein (WASP)-deficient mice. In addition, they found that both endogenous and exogenous IAP is important as intestinal inflammation in both wild-type and IAP-gene knockout models was attenuated after oral administration of calf IAP. A recent clinical study showed that naso-duodenal administration of IAP could benefit patients with active UC [3].