Deficiency of Intestinal α1-2-Fucosylation Exacerbates Ethanol-Induced Liver Disease in Mice.

摘要: Background Fucosyltransferase 2 (Fut2)-mediated intestinal α1-2-fucosylation is important in maintaining a symbiotic host-microbiota relationship and can protect against several pathogens. Intestinal dysbiosis an factor for the progression of experimental ethanol (EtOH)-induced liver disease, but role Fut2 modulating glycocalyx during alcohol-associated disease unknown. We investigated Fut2-mediated development disease. Methods Immunohistochemistry staining was applied to evaluate duodenal biopsies from patients with alcohol use disorder. Wild-type (WT) Fut2-deficient littermate mice were subjected Lieber-DeCarli models chronic EtOH administration chronic-binge diet (NIAAA model). Results down-regulated Lack exacerbates EtOH-induced injury, steatosis, inflammation without affecting metabolism. Dietary supplementation α1-2-fucosylated glycan 2'-fucosyllactose (2'-FL) ameliorates NIAAA model. Despite no direct effects on growth Enterococcus faecalis vitro, reduces colonization cytolysin-positive E. intestine EtOH-fed mice. Conclusions acts as host-protective mechanism 2'-FL oligosaccharide naturally present human milk that could be considered therapeutic agent