Sa2032 Salmonella Infection Inhibits Intestinal Biotin Uptake: Cellular/Molecular Mechanisms

Abstract

non-invasively by oral administration of multiple sugar probes and, subsequently, assessing the excretion of these probes in urine. This test was conducted prior to and after intervention in the absence and, on separate test days, in the presence of an indomethacin challenge. The non-steroidal anti-inflammatory drug indomethacin has been shown to induce reversible damage to the upper gastrointestinal tract, and was applied as a model to study the effects of the supplementation on compromised intestinal barrier function. Results: Gastroduodenal and small intestinal permeability were significantly increased in the indomethacin stressed condition, compared with the unstressed condition, as assessed by urinary sucrose recovery (0.248 [0.206-0.318] vs. 0.363 [0.291-0.637] P<0.05) and urinary lactulose/rhamnose excretion ratio (0.047 [0.039-0.069] vs. 0.118 [0.082-0.165] P<0.001). Indomethacin did not affect colonic permeability as determined by sucralose/erythritol excretion ratio. The synbiotic supplementation did not affect gastroduodenal, small intestinal, and colonic permeability as reflected by urinary sucrose recovery, lactulose/rhamnose excretion ratio and sucralose/ erythritol excretion ratio, respectively. These findings were not different among the stressed and unstressed conditions. Conclusion: We confirmed that indomethacin causes damage to the stomach and small intestine. Further, we conclude that two weeks supplementation of scFOS+Ecologic® 825 does not reinforce gastroduodenal, small intestinal or colonic permeability in a healthy gut, nor in a compromised gut.