Enteral Nntrition Promotes The Remission Of Colitis By Gut Microbes-Mediated Histidine Biosynthesis

Exclusive enteral nutrition is an important alternative strategy for Crohns disease patients. Although alterations of microbiota have been observed in CD patients with EEN treatment, the underlying mechanisms by which EEN reduce intestinal inflammation still remain unclear. Therapeutic potential of enteral nutrition therapy was observed in both the dextran sulfate sodium induced colitis and spontaneous colitis mice models. Accumulation of Faecalibaculum rodentium after EN therapy was found by full-length 16S rDNA sequencing and verified by several metagenome datasets from CD patients. Colonization of an isolated F. rodentium was able to reduce the colitis in the spontaneous colitis mice model. Significant histidine enrichment was observed in the F. rodentium culture supernatant, and a series of histidine biosynthesis genes were also observed in the F. rodentium genome. Engineered Escherichia coli Nissle 1917, encoding heterologous hisG of F. rodentium, a key driver of histidine biosynthesis of F. rodentium, protected against colitis in mice.This study suggests that EN-induced F. rodentium accumulation protects against colitis via gut microbe-mediated histidine biosynthesis.