Figure 1: Hypothetical model depicting the mechanism by which a brush border enzyme intestinal alkaline phosphatase (IAP) affects the intestinal microbiota, the release of bacterial LPS-induced inflammation, and the luminal content of ATP inhibiting the commensal bacteria of different origin. Under inflammation, the proinflammatory cytokines can inhibit the content and activity of protective IAP. The IAP can dephosphorylate bacterial LPS which leads to LPS detoxification, thus preventing downstream activation of immunocytes and the subsequent inflammatory responses. The IAP can inhibit luminal ATP by the mechanism involving the ATP dephosphorylation. This enzyme was found to exert an inhibitory effect on the growth and survival of a wide spectrum of bacteria and to prevent bacteria translocation from intestinal lumen into bloodstream. The mechanisms illustrated in this figure which are described in the text were inspired by [8, 9] cited in this review.