Methyl donor microbiome mice Targeted Locus (Loci). mouse gut metagenome

Increasing number of observations indicate that the intestinal microbiota plays an etiologic role in inflammatory bowel diseases (IBD). Transient postnatal changes in gut microbiota composition have been shown to modulate predisposition to intestinal inflammation in murine models of IBD. However, the effects of environmental influences on prenatal developmental programming in respect to postnatal micobiome composition and predilection towards mammalian colitis have not been examined. Here we tested how prenatal methyl donor (MD) supplementation modifies young adult microbiome structure and acute colitis susceptibility in mice. The fetal nutritional intervention induced a colitogenic microbiome separation in the offspring. The findings of this work support that prenatal metabolic imprinting can induce the nurturing of a colitogenic microbiome in mammals. These results may have translational relevance in regards to the developmental origins of human IBD.