报告人简介：
Dr Jean-Paul Lallès is biochemist, agriculture engineer, physiologist, immunologist and PhD in animal nutrition.报告内容：
Intestinal alkaline phosphatase (IAP) is predominantly expressed in and produced by the small intestine (enterocyte) of both terrestrial mammals and aquatic vertebrates. It displays diverse homeostatic functions, including regulation of enterocyte surface pH, fatty acid absorption, detoxification (by dephosphorylation) of free nucleotides and bacterial components (e.g. lipopolysaccharide, flagellin, CpG DNA motifs), down-regulation of NFkB signaling and subsequent reduction of local (and systemic) inflammation (1,2). IAP directly participates in gut barrier maintenance at the tight junction protein level (3). It also directly contributes to the resolution of intestinal inflammation through e.g. resolvin-E1 (a molecule derived from omega 3 PUFA). IAP enzyme partially resists digestion and degradation in the small and large intestines, thus contributing to control inflammation also in the colon, and a still active fraction of IAP is found in the faeces. Recent data indicate that IAP shapes the gut microbiota indirectly by dephosphorylating luminal adenosine triphosphate (ATP) and other inflammatory nucleotide triphosphates (2,3). Endogenous IAP favours bacterial growth but is able to downregulate IL-8 production induced by Gram-negative bacteria (E. coli; S. enterolytica Typhymurium) but not by Gram-positive bacteria. Conversely, extracellular ATP, a danger signal specifically inhibits the growth of Gram-positive bacteria. Thus IAP mediates microbiota balance in the gut. In terms of prevention or treatment, exogenous IAP (e.g. from bovine intestine) has been shown in all the published studies to reduce inflammation in various animal models (colitis, peritonitis, sepsis) and in humans (ulcerative colitis, coronary surgery and chronic kidney disease), showing its strong anti-inflammatory power. IAP can also prevent and reverse diet-induced type-2 diabetes, insulin resistance, dyslipidemia and metabolic syndrome in mice, thus showing its role in the control of low-grade (metabolic) inflammation. Stimulating endogenous IAP expression and activity can be achieved by many dietary nutrients and components, making the diet a potent lever for keeping a healthy gut and microbiota composition. In conclusion, IAP is a fundamental anti-inflammatory mechanism highly conserved across species, and nutrition is a major lever for controlling inflammation through IAP.